Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous membranes and used as a topical antiseptic and disinfectant.
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
The normal lack of the ability to produce an immunological response to autologous (self) antigens. A breakdown of self tolerance leads to autoimmune diseases. The ability to recognize the difference between self and non-self is the prime function of the immune system.
CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.
The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.
Inflammatory disease of the THYROID GLAND due to autoimmune responses leading to lymphocytic infiltration of the gland. It is characterized by the presence of circulating thyroid antigen-specific T-CELLS and thyroid AUTOANTIBODIES. The clinical signs can range from HYPOTHYROIDISM to THYROTOXICOSIS depending on the type of autoimmune thyroiditis.
A strain of non-obese diabetic mice developed in Japan that has been widely studied as a model for T-cell-dependent autoimmune insulin-dependent diabetes mellitus in which insulitis is a major histopathologic feature, and in which genetic susceptibility is strongly MHC-linked.
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
A mouse substrain that is genetically predisposed to the development of systemic lupus erythematosus-like syndrome, which has been found to be clinically similar to the human disease. It has been determined that this mouse strain carries a mutation in the fas gene. Also, the MRL/lpr is a useful model to study behavioral and cognitive deficits found in autoimmune diseases and the efficacy of immunosuppressive agents.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)
Disorders caused by cellular or humoral immune responses primarily directed towards nervous system autoantigens. The immune response may be directed towards specific tissue components (e.g., myelin) and may be limited to the central nervous system (e.g., MULTIPLE SCLEROSIS) or the peripheral nervous system (e.g., GUILLAIN-BARRE SYNDROME).
A pyridoxal-phosphate protein that catalyzes the alpha-decarboxylation of L-glutamic acid to form gamma-aminobutyric acid and carbon dioxide. The enzyme is found in bacteria and in invertebrate and vertebrate nervous systems. It is the rate-limiting enzyme in determining GAMMA-AMINOBUTYRIC ACID levels in normal nervous tissues. The brain enzyme also acts on L-cysteate, L-cysteine sulfinate, and L-aspartate. EC 4.1.1.15.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.
Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (IMMUNOTHERAPY, ADOPTIVE).
A proinflammatory cytokine produced primarily by T-LYMPHOCYTES or their precursors. Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene.
Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Theoretical representations that simulate the behavior or activity of immune system, processes, or phenomena. They include the use of mathematical equations, computers, and other electrical equipment.
A subclass of winged helix DNA-binding proteins that share homology with their founding member fork head protein, Drosophila.
A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).
Autoimmune diseases affecting multiple endocrine organs. Type I is characterized by childhood onset and chronic mucocutaneous candidiasis (CANDIDIASIS, CHRONIC MUCOCUTANEOUS), while type II exhibits any combination of adrenal insufficiency (ADDISON'S DISEASE), lymphocytic thyroiditis (THYROIDITIS, AUTOIMMUNE;), HYPOPARATHYROIDISM; and gonadal failure. In both types organ-specific ANTIBODIES against a variety of ENDOCRINE GLANDS have been detected. The type II syndrome differs from type I in that it is associated with HLA-A1 and B8 haplotypes, onset is usually in adulthood, and candidiasis is not present.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
An encapsulated lymphatic organ through which venous blood filters.
Antibodies specific to INSULIN.
A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.
Subset of helper-effector T-lymphocytes which synthesize and secrete IL-17, IL-17F, and IL-22. These cytokines are involved in host defenses and tissue inflammation in autoimmune diseases.
A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.
A tumor necrosis factor superfamily member that plays a role in the regulation of B-LYMPHOCYTE survival. It occurs as a membrane-bound protein that is cleaved to release an biologically active soluble form with specificity to TRANSMEMBRANE ACTIVATOR AND CAML INTERACTOR PROTEIN; B-CELL ACTIVATION FACTOR RECEPTOR; and B-CELL MATURATION ANTIGEN.
A single, unpaired primary lymphoid organ situated in the MEDIASTINUM, extending superiorly into the neck to the lower edge of the THYROID GLAND and inferiorly to the fourth costal cartilage. It is necessary for normal development of immunologic function early in life. By puberty, it begins to involute and much of the tissue is replaced by fat.
A subtype of non-receptor protein tyrosine phosphatases that is characterized by the presence of an N-terminal catalytic domain and a C-terminal PROLINE-rich domain. The phosphatase subtype is predominantly expressed in LYMPHOCYTES and plays a key role in the inhibition of downstream T-LYMPHOCYTE activation. Polymorphisms in the gene that encodes this phosphatase subtype are associated with a variety of AUTOIMMUNE DISEASES.
Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.
Chronic autoimmune thyroiditis, characterized by the presence of high serum thyroid AUTOANTIBODIES; GOITER; and HYPOTHYROIDISM.
Molecules on the surface of T-lymphocytes that recognize and combine with antigens. The receptors are non-covalently associated with a complex of several polypeptides collectively called CD3 antigens (ANTIGENS, CD3). Recognition of foreign antigen and the major histocompatibility complex is accomplished by a single heterodimeric antigen-receptor structure, composed of either alpha-beta (RECEPTORS, ANTIGEN, T-CELL, ALPHA-BETA) or gamma-delta (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA) chains.
A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
The structure of one molecule that imitates or simulates the structure of a different molecule.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
Thyroglobulin is a protein produced by thyroid cells that is used to diagnose and monitor thyroid cancer.
A classification of B-lymphocytes based on structurally or functionally different populations of cells.
An inhibitory T CELL receptor that is closely related to CD28 ANTIGEN. It has specificity for CD80 ANTIGEN and CD86 ANTIGEN and acts as a negative regulator of peripheral T cell function. CTLA-4 antigen is believed to play role in inducing PERIPHERAL TOLERANCE.
A hemeprotein that catalyzes the oxidation of the iodide radical to iodine with the subsequent iodination of many organic compounds, particularly proteins. EC 1.11.1.8.
Reduction in the number of lymphocytes.
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
Pathological processes involving the THYROID GLAND.
A group of the D-related HLA antigens found to differ from the DR antigens in genetic locus and therefore inheritance. These antigens are polymorphic glycoproteins comprising alpha and beta chains and are found on lymphoid and other cells, often associated with certain diseases.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.
The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.
B-cells that have a role in regulating the immune response including the production of CYTOKINES. This function is in addition to their traditional role in making antibodies.
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
Transmembrane proteins that form the beta subunits of the HLA-DQ antigens.
A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.
Enlargement of the spleen.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A fibrillar collagen found widely distributed as a minor component in tissues that contain COLLAGEN TYPE I and COLLAGEN TYPE III. It is a heterotrimeric molecule composed of alpha1(V), alpha2(V) and alpha3(V) subunits. Several forms of collagen type V exist depending upon the composition of the subunits that form the trimer.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).
The mechanism, in peripheral lymphoid organs (LYMPH NODES; SPLEEN; TONSILS; and mucosal-associated lymphoid tissue), that prevents mature lymphocytes from reacting to SELF-ANTIGENS. This is accomplished through a variety of means including CLONAL ANERGY and CLONAL DELETION.
The process by which antigen is presented to lymphocytes in a form they can recognize. This is performed by antigen presenting cells (APCs). Some antigens require processing before they can be recognized. Antigen processing consists of ingestion and partial digestion of the antigen by the APC, followed by presentation of fragments on the cell surface. (From Rosen et al., Dictionary of Immunology, 1989)
The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
Mouse strains constructed to possess identical genotypes except for a difference at a single gene locus.
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Mice bearing mutant genes which are phenotypically expressed in the animals.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A transmembrane protein present in the MYELIN SHEATH of the CENTRAL NERVOUS SYSTEM. It is one of the main autoantigens implicated in the pathogenesis of MULTIPLE SCLEROSIS.
A low affinity interleukin-2 receptor subunit that combines with the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN to form a high affinity receptor for INTERLEUKIN-2.
Chronic inflammatory and autoimmune disease in which the salivary and lacrimal glands undergo progressive destruction by lymphocytes and plasma cells resulting in decreased production of saliva and tears. The primary form, often called sicca syndrome, involves both KERATOCONJUNCTIVITIS SICCA and XEROSTOMIA. The secondary form includes, in addition, the presence of a connective tissue disease, usually rheumatoid arthritis.
An excess of GAMMA-GLOBULINS in the serum due to chronic infections or PARAPROTEINEMIAS.
Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.
Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection.
A subclass of receptor-like protein tryosine phosphatases that contain an extracellular RDGS-adhesion recognition motif and a single cytosolic protein tyrosine phosphate domain.
An abundant cytosolic protein that plays a critical role in the structure of multilamellar myelin. Myelin basic protein binds to the cytosolic sides of myelin cell membranes and causes a tight adhesion between opposing cell membranes.
Alteration of the immune system or of an immune response by agents that activate or suppress its function. This can include IMMUNIZATION or administration of immunomodulatory drugs. Immunomodulation can also encompass non-therapeutic alteration of the immune system effected by endogenous or exogenous substances.
The body's defense mechanism against foreign organisms or substances and deviant native cells. It includes the humoral immune response and the cell-mediated response and consists of a complex of interrelated cellular, molecular, and genetic components.
Inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (sclera and cornea, and the retina). (Dorland, 27th ed)
Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
Surgical removal of the thymus gland. (Dorland, 28th ed)
Inflammatory diseases of the THYROID GLAND. Thyroiditis can be classified into acute (THYROIDITIS, SUPPURATIVE), subacute (granulomatous and lymphocytic), chronic fibrous (Riedel's), chronic lymphocytic (HASHIMOTO DISEASE), transient (POSTPARTUM THYROIDITIS), and other AUTOIMMUNE THYROIDITIS subtypes.
A heterogeneous group of immunocompetent cells that mediate the cellular immune response by processing and presenting antigens to the T-cells. Traditional antigen-presenting cells include MACROPHAGES; DENDRITIC CELLS; LANGERHANS CELLS; and B-LYMPHOCYTES. FOLLICULAR DENDRITIC CELLS are not traditional antigen-presenting cells, but because they hold antigen on their cell surface in the form of IMMUNE COMPLEXES for B-cell recognition they are considered so by some authors.
A condition characterized by persistent spasms (SPASM) involving multiple muscles, primarily in the lower limbs and trunk. The illness tends to occur in the fourth to sixth decade of life, presenting with intermittent spasms that become continuous. Minor sensory stimuli, such as noise and light touch, precipitate severe spasms. Spasms do not occur during sleep and only rarely involve cranial muscles. Respiration may become impaired in advanced cases. (Adams et al., Principles of Neurology, 6th ed, p1492; Neurology 1998 Jul;51(1):85-93)
ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN.
Sites on an antigen that interact with specific antibodies.
Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.
Invasion of the host organism by microorganisms that can cause pathological conditions or diseases.
Protection from an infectious disease agent that is mediated by B- and T- LYMPHOCYTES following exposure to specific antigen, and characterized by IMMUNOLOGIC MEMORY. It can result from either previous infection with that agent or vaccination (IMMUNITY, ACTIVE), or transfer of antibody or lymphocytes from an immune donor (IMMUNIZATION, PASSIVE).
Antibodies produced by a single clone of cells.
A strain of Rattus norvegicus which is a model for spontaneous insulin-dependent diabetes mellitus (DIABETES MELLITUS, INSULIN-DEPENDENT).
A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
Disorders characterized by proliferation of lymphoid tissue, general or unspecified.
Diseases of LYMPH; LYMPH NODES; or LYMPHATIC VESSELS.
Receptors present on activated T-LYMPHOCYTES and B-LYMPHOCYTES that are specific for INTERLEUKIN-2 and play an important role in LYMPHOCYTE ACTIVATION. They are heterotrimeric proteins consisting of the INTERLEUKIN-2 RECEPTOR ALPHA SUBUNIT, the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT, and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.
Syndromes in which there is a deficiency or defect in the mechanisms of immunity, either cellular or humoral.
Substances that are recognized by the immune system and induce an immune reaction.
Functional inactivation of T- or B-lymphocytes rendering them incapable of eliciting an immune response to antigen. This occurs through different mechanisms in the two kinds of lymphocytes and can contribute to SELF TOLERANCE.
A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-23 is comprised of a unique 19 kDa subunit and 40 kDa subunit that is shared with INTERLEUKIN-12. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cells
Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation.
A subclass of HLA-D antigens that consist of alpha and beta chains. The inheritance of HLA-DR antigens differs from that of the HLA-DQ ANTIGENS and HLA-DP ANTIGENS.
Antigens expressed primarily on the membranes of living cells during sequential stages of maturation and differentiation. As immunologic markers they have high organ and tissue specificity and are useful as probes in studies of normal cell development as well as neoplastic transformation.
The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.
Deliberate breeding of two different individuals that results in offspring that carry part of the genetic material of each parent. The parent organisms must be genetically compatible and may be from different varieties or closely related species.
Arthritis is a medical condition characterized by inflammation and degeneration of the joints, causing pain, stiffness, and reduced mobility.
A medical specialty concerned with the hypersensitivity of the individual to foreign substances and protection from the resultant infection or disorder.
Removal, via CELL DEATH, of immature lymphocytes that interact with antigens during maturation. For T-lymphocytes this occurs in the thymus and ensures that mature T-lymphocytes are self tolerant. B-lymphocytes may also undergo clonal deletion.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.
Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role.
IMMUNOGLOBULINS on the surface of B-LYMPHOCYTES. Their MESSENGER RNA contains an EXON with a membrane spanning sequence, producing immunoglobulins in the form of type I transmembrane proteins as opposed to secreted immunoglobulins (ANTIBODIES) which do not contain the membrane spanning segment.
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.
The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.
A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to MERCURY POISONING. Because of its toxicity, the clinical use of mercury and mercurials is diminishing.
Antigenic determinants recognized and bound by the T-cell receptor. Epitopes recognized by the T-cell receptor are often located in the inner, unexposed side of the antigen, and become accessible to the T-cell receptors after proteolytic processing of the antigen.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.
The number of LYMPHOCYTES per unit volume of BLOOD.
T-cell receptors composed of CD3-associated alpha and beta polypeptide chains and expressed primarily in CD4+ or CD8+ T-cells. Unlike immunoglobulins, the alpha-beta T-cell receptors recognize antigens only when presented in association with major histocompatibility (MHC) molecules.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.
A member of the tumor necrosis factor receptor superfamily that specifically binds B-CELL ACTIVATING FACTOR. It is found on B-LYMPHOCYTES and plays a role in maturation and survival of B-cells. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
55-kDa antigens found on HELPER-INDUCER T-LYMPHOCYTES and on a variety of other immune cell types. CD4 antigens are members of the immunoglobulin supergene family and are implicated as associative recognition elements in MAJOR HISTOCOMPATIBILITY COMPLEX class II-restricted immune responses. On T-lymphocytes they define the helper/inducer subset. CD4 antigens also serve as INTERLEUKIN-15 receptors and bind to the HIV receptors, binding directly to the HIV ENVELOPE PROTEIN GP120.
Antibody-mediated immune response. Humoral immunity is brought about by ANTIBODY FORMATION, resulting from TH2 CELLS activating B-LYMPHOCYTES, followed by COMPLEMENT ACTIVATION.
Loss of scalp and body hair involving microscopically inflammatory patchy areas.
A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
The activated center of a lymphoid follicle in secondary lymphoid tissue where B-LYMPHOCYTES are stimulated by antigens and helper T cells (T-LYMPHOCYTES, HELPER-INDUCER) are stimulated to generate memory cells.
A costimulatory ligand expressed by ANTIGEN-PRESENTING CELLS that binds to CTLA-4 ANTIGEN with high specificity and to CD28 ANTIGEN with low specificity. The interaction of CD80 with CD28 ANTIGEN provides a costimulatory signal to T-LYMPHOCYTES, while its interaction with CTLA-4 ANTIGEN may play a role in inducing PERIPHERAL TOLERANCE.
The altered state of immunologic responsiveness resulting from initial contact with antigen, which enables the individual to produce antibodies more rapidly and in greater quantity in response to secondary antigenic stimulus.
The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.
Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.
Conditions characterized by loss or dysfunction of myelin (see MYELIN SHEATH) in the brain, spinal cord, or optic nerves secondary to autoimmune mediated processes. This may take the form of a humoral or cellular immune response directed toward myelin or OLIGODENDROGLIA associated autoantigens.
Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort T-lymphocytes into subsets based on CD antigens by the technique of flow cytometry.
A general term for diseases produced by viruses.
Glycoproteins found on the membrane or surface of cells.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.
A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ANTIGENS on B-LYMPHOCYTES and induces their proliferation. Mutation of the gene for CD40 ligand is a cause of HYPER-IGM IMMUNODEFICIENCY SYNDROME, TYPE 1.
An induced state of non-reactivity to grafted tissue from a donor organism that would ordinarily trigger a cell-mediated or humoral immune response.
A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.

Fine specificity of the autoimmune response to the Ro/SSA and La/SSB ribonucleoproteins. (1/3192)

The fine specificity of the Ro and La proteins has been studied by several techniques. In general, there is agreement in a qualitative sense that autoantibodies bind multiple epitopes. For some specific antibody binding, different studies agree quantitatively, for instance, the binding of the carboxyl terminus of 60-kd Ro as described by 2 studies using different techniques and the presence of an epitope within the leucine zipper of 52-kd Ro. In addition, there is general agreement about the location of a prominent epitope at the RRM motif region of the La molecule. On the other hand, the many specific epitope regions of the molecules differ among these studies. These discrepancies are likely the result of using different techniques, sera, and peptide constructs as well as a result of inherent advantages and disadvantages in the individual approaches. Several theories concerning the origin of not only the antibodies, but also the diseases themselves, have been generated from studies of the fine specificity of antibody binding. These include a theory of a primordial foreign antigen for anti-Ro autoimmunity, molecular mimicry with regard to La and CCHB, as well as the association of anti-Ro with HLA. These remain unproven, but are of continuing interest. An explanation for the association of anti-60-kd Ro and anti-52-kd Ro in the sera of patients has sprung from evaluating antibody binding. Data demonstrating multiple epitopes are part of a large body of evidence that strongly suggests an antigen-driven immune response. This means that the autoantigens are directly implicated in initiating and sustaining autoimmunity in their associated diseases. A number of studies have investigated the possibility of differences in the immune response to these antigens in SS and SLE sera. While several differences have been reported, none have been reproduced in a second cohort of patients. Furthermore, none of the reported differences may be sufficiently robust for clinical purposes, such as distinguishing between SS with systemic features and mild SLE, although some might be promising. For instance, in at least 3 groups of SLE patients, no binding of residues spanning amino acids 21-41 of 60-kd Ro has been found. Meanwhile, 1 of those studies found that 41% of sera from patients with primary SS bound the 60-kd Ro peptide 21-41. Perhaps future studies will elaborate a clinical role of such a difference among SS and SLE patients. Study of the epitopes of these autoantigens has, in part, led to a new animal model of anti-Ro and anti-La. Non-autoimmune-prone animals are immunized with proteins or peptides that make up the Ro/La RNP. Such animals develop an autoimmune response to the entire particle, not just the immunogen. This response has been hypothesized to arise from autoreactive B cells. In another, older animal model of disease, the MRL-lpr/lpr mouse, B cells have recently been shown to be required for the generation of abnormal, autoreactive T cells. Thus, there are now powerful data indicating that B cells that produce autoantibodies are directly involved in the pathogenesis of disease above and beyond the formation of immune complexes. Given that the autoreactive B cell is potentially critical to the underlying pathogenesis of disease, then studying these cells will be crucial to further understanding the origin of diseases associated with Ro and La autoimmunity. Hopefully, an increased understanding will eventually lead to improved treatment of patients. Progress in the area of treatment will almost surely be incremental, and studies of the fine specificity of autoantibody binding will be a part of the body of basic knowledge contributing to ultimate advancement. In the future, the animal models will need to be examined with regard to immunology and immunochemistry as well as genetics. The development of these autoantibodies has not been studied extensively because upon presentation to medical care, virtually all patients have a full-  (+info)

Development and function of autospecific dual TCR+ T lymphocytes. (2/3192)

Recent studies have challenged the long held concept that each T lymphocyte expresses on its surface only a single, unique alphabetaTCR. Dual TCR+ T cells have been recognized, however, their origin and potential to escape screening for self-reactivity remain obscure. We now report the thymic generation of dual alphabetaTCR+ T cells in the H-2Db/H-Y-specific TCR transgenic (Tg) mouse. Dual TCR+ thymocytes were positively selected less efficiently than single TCR+ thymocytes, although a subset attained maturity. Importantly, when TCR Tg mice were bred onto a negatively selecting background, auto-specific cells survived central deletion and matured as CD4+ dual TCR+ cells. These cells were autoreactive when CD8 expression was restored. The existence of autospecific, dual TCR+ T cells may have implications for the maintenance of self tolerance.  (+info)

Induction of autoimmunity by multivalent immunodominant and subdominant T cell determinants of La (SS-B). (3/3192)

We investigated the consequences of altering the form and valence of defined autodeterminants on the initiation and spreading of experimentally induced La/Ro autoimmunity. Anti-La and Ro (SS-A) Ab responses were monitored following immunization of healthy mice with defined immunodominant and subdominant T cell determinants of the La (SS-B) autoantigen synthesized as either monomeric or multiple antigenic (MAP) peptides. Abs to mouse La (mLa) developed faster and were of higher titer in mice immunized with the subdominant mLa25-44 MAP compared with mice immunized with the 25-44 monomer. Rapid intermolecular spreading of the autoimmune response to 60-kDa Ro was observed in AKR/J mice immunized with mLa25-44 MAP, but not in mice immunized repeatedly with monomeric peptide. A/J mice immunized and boosted with the known tolerogenic mLa287-301 determinant delivered as monomeric peptide failed to develop Abs to either intact mLa or mLa287-301 peptide. However, immunization with the multivalent mLa287-301 peptide led to the rapid production of high titer mLa autoantibodies associated with a proliferative T cell response to the mLa287-301 peptide. The data suggested that the enhanced immunogenicity of MAPs was not due to augmented Ag presentation or T cell stimulation. However, MAP-, but not monomer peptide-, containing immune complexes were potent substrates for Ab-dependent fixation of complement. These results demonstrate that the form of Ag responsible for inducing autoimmunity can profoundly influence the nature and magnitude of the immune response. Thus, molecular mimicry of tolerogenic and nontolerogenic self determinants might trigger autoimmunity under conditions of altered valence.  (+info)

Clinical, biochemical and molecular genetic features of Leber's hereditary optic neuropathy. (4/3192)

Leber's hereditary optic neuropathy (LHON) has traditionally been considered a disease causing severe and permanent visual loss in young adult males. In nearly all families with LHON it is associated with one of three pathogenic mitochondrial DNA (mtDNA) mutations, at bp 11778, 3460 or 14484. The availability of mtDNA confirmation of a diagnosis of LHON has demonstrated that LHON occurs with a wider range of age at onset and more commonly in females than previously recognised. In addition, analysis of patients grouped according to mtDNA mutation has demonstrated differences both in the clinical features of visual failure and in recurrence risks to relatives associated with each of the pathogenic mtDNA mutations. Whilst pathogenic mtDNA mutations are required for the development of LHON, other factors must be reponsible for the variable penetrance and male predominance of this condition. Available data on a number of hypotheses including the role of an additional X-linked visual loss susceptibility locus, impaired mitochondrial respiratory chain activity, mtDNA heteroplasmy, environmental factors and autoimmunity are discussed. Subacute visual failure is seen in association with all three pathogenic LHON mutations. However, the clinical and experimental data reviewed suggest differences in the phenotype associated with each of the three mutations which may reflect variation in the disease mechanisms resulting in this common end-point.  (+info)

Vaccination with a recombinant vaccinia virus encoding a "self" antigen induces autoimmune vitiligo and tumor cell destruction in mice: requirement for CD4(+) T lymphocytes. (5/3192)

Many human and mouse tumor antigens are normal, nonmutated tissue differentiation antigens. Consequently, immunization with these "self" antigens could induce autoimmunity. When we tried to induce immune responses to five mouse melanocyte differentiation antigens, gp100, MART-1, tyrosinase, and tyrosinase-related proteins (TRP) 1 and TRP-2, we observed striking depigmentation and melanocyte destruction only in the skin of mice inoculated with a vaccinia virus encoding mouse TRP-1. These mice rejected a lethal challenge of B16 melanoma, indicating the immune response against TRP-1 could destroy both normal and malignant melanocytes. Cytotoxic T lymphocytes specific for TRP-1 could not be detected in depigmented mice, but high titers of IgG anti-TRP-1 antibodies were present. Experiments with knockout mice revealed an absolute dependence on major histocompatibility complex class II, but not major histocompatibility complex class I, for the induction of both vitiligo and tumor protection. Together, these results suggest that the deliberate induction of self-reactivity using a recombinant viral vector can lead to tumor destruction, and that in this model, CD4(+) T lymphocytes are an integral part of this process. Vaccine strategies targeting tissue differentiation antigens may be valuable in cancers arising from nonessential cells and organs such as melanocytes, prostate, testis, breast, and ovary.  (+info)

Autoimmunity resulting from cytokine treatment predicts long-term survival in patients with metastatic renal cell cancer. (6/3192)

PURPOSE: In patients undergoing cytokine therapy, systemically applied interleukin-2 (IL-2) and/or interferon-alpha (IFN-alpha) have been reported to induce thyroid dysfunction as well as thyroid autoantibodies. We analyzed the correlation of thyroid autoimmunity with HLA phenotype, various other autoimmune parameters, and patient survival. PATIENTS AND METHODS: For this purpose, antithyroglobulin autoantibodies, antimicrosomal thyroid autoantibodies, thyroglobulin receptor autoantibodies, thyroid dysfunction, and multiple clinical parameters were determined in 329 unselected patients with metastatic renal cell cancer before and after systemic IL-2 and IFN-alpha2 therapy. For statistical analysis, we used both univariate and multivariate Cox proportional hazards models and the two-tailed Fisher's exact test. RESULTS: Antithyroglobulin autoantibodies and antimicrosomal thyroid autoantibodies were detected in 60 patients (18%); positive autoantibody titers of various other autoimmune parameters were statistically unrelated. The presence of thyroid autoantibodies was correlated with prolonged survival (P<.0001). There was a statistically significant difference in frequencies of HLA-Cw7 expression between thyroid autoantibody-positive and -negative patients (P< or =.05), and the Cw7 expression was associated with prolonged overall survival (P = .009). CONCLUSION: The evaluation of thyroid autoantibodies during cytokine therapy could be a useful prognostic marker for patients with renal cell carcinoma who benefit from cytokine treatment. IL-2- and IFN-alpha2-induced tumor control and prolonged survival may require breaking of immunologic tolerance against self-antigens.  (+info)

Evidence of cell-mediated cardiac myocyte injury involved in the heart failure of a patient with progressive systemic sclerosis. (7/3192)

A 54-year-old woman with progressive systemic sclerosis (PSS) was admitted to hospital because of dyspnea and chest pain. Echocardiogram revealed diffuse hypokinesis of the left ventricle (ejection fraction 24%). Methylprednisolone, heparin, and diuretics were administered, without benefit. Anemia, thrombocytopenia, and renal dysfunction rapidly progressed, and she died of heart failure on the 14th hospital day. Immunohistochemical study of the myocardial tissue showed mild to moderate cell infiltration, mainly consisting of natural killer (NK) cells, macrophages, cytotoxic T lymphocytes (CTLs), and T helper cells. Perforin, a cytolytic factor, was expressed in the infiltrating CTLs and NK cells, indicating that these cells were activated killer cells. Furthermore, human leukocyte antigen classes I and II, intercellular adhesion molecule-1, as well as costimulatory molecules B7-1, B7-2, and CD40, all of which are known not to be expressed in cardiac myocytes under normal conditions, were moderately to strongly expressed in cardiac myocytes. There was no detectable level of enterovirus genomes in the polymerase chain reaction products from the myocardial tissue of this patient. These findings strongly suggest that the infiltrating killer cells recognized cardiac myocytes as target cells and directly damaged them by releasing perforin. Enhanced expression of these antigens may have played an important role in the activation and cytotoxicity of the infiltrating killer cells. Absence of enterovirus genomes in the myocardial tissue may suggest that this autoimmune process is primarily induced by PSS.  (+info)

Clinical presentation and early course of type 1 diabetes in patients with and without thyroid autoimmunity. (8/3192)

OBJECTIVE: To evaluate the prevalence of thyroid autoimmunity (TAI) in patients with recent-onset type 1 diabetes and to determine the influence of TAI on the clinical presentation and evolution of type 1 diabetes. RESEARCH DESIGN AND METHODS: We studied 111 newly diagnosed type 1 diabetes patients > 13 years old. The diagnosis of TAI was based on medical history and measurement of thyroid peroxidase (microsomal) antibodies (TPOAs). Clinical presentation of diabetes, beta-cell autoimmune markers (GADAs and 1A2As), and evolution of insulin-secretory reserves and metabolic control during the first 2 years of follow-up were analyzed. Differences between groups were evaluated by Student's t test or the chi 2 test. The influence of TAI on follow-up data was evaluated by multiple logistic regression analysis. RESULTS: TAI was present in 31 patients (14 TPOA+ patients with normal thyroid function, 12 TPOA+ patients with thyroid dysfunction, and 5 patients with previously diagnosed TAI). TAI was more prevalent in women than in men (43.7 vs. 15.9%, P = 0.001). beta-Cell autoimmunity was more prevalent in patients with TAI than in those without TAI (93.5 vs. 76.3%, P = 0.03). The evolution of insulin requirements, metabolic control, and insulin-secretory reserves was comparable in the two groups. CONCLUSIONS: TAI is present in many type 1 diabetes patients at the time of diagnosis and is associated with a high prevalence of thyroid dysfunction. The clinical presentation of diabetes and the evolution of metabolic control and insulin-secretory reserves are not influenced by the presence of TAI. Patients with type 1 diabetes should be screened for TAI at diagnosis.  (+info)

Autoimmune diseases are a group of disorders in which the immune system mistakenly attacks healthy cells and tissues in the body. In a healthy immune system, the body recognizes and attacks foreign substances, such as viruses and bacteria, to protect itself. However, in autoimmune diseases, the immune system becomes overactive and begins to attack the body's own cells and tissues. There are over 80 different types of autoimmune diseases, and they can affect various parts of the body, including the joints, skin, muscles, blood vessels, and organs such as the thyroid gland, pancreas, and liver. Some common examples of autoimmune diseases include rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, and inflammatory bowel disease. The exact cause of autoimmune diseases is not fully understood, but it is believed to involve a combination of genetic and environmental factors. Treatment for autoimmune diseases typically involves managing symptoms and reducing inflammation, and may include medications, lifestyle changes, and in some cases, surgery.

Autoantibodies are antibodies that are produced by the immune system against the body's own cells, tissues, or organs. In other words, they are antibodies that mistakenly target and attack the body's own components instead of foreign invaders like viruses or bacteria. Autoantibodies can be present in people with various medical conditions, including autoimmune diseases such as rheumatoid arthritis, lupus, and multiple sclerosis. They can also be found in people with certain infections, cancer, and other diseases. Autoantibodies can cause damage to the body's own cells, tissues, or organs, leading to inflammation, tissue destruction, and other symptoms. They can also interfere with the normal functioning of the body's systems, such as the nervous system, digestive system, and cardiovascular system. Diagnosis of autoantibodies is typically done through blood tests, which can detect the presence of specific autoantibodies in the blood. Treatment for autoimmune diseases that involve autoantibodies may include medications to suppress the immune system, such as corticosteroids or immunosuppressants, as well as other therapies to manage symptoms and prevent complications.

Diabetes Mellitus, Type 1 is a chronic metabolic disorder characterized by high blood sugar levels due to the body's inability to produce insulin, a hormone that regulates blood sugar levels. This type of diabetes is also known as insulin-dependent diabetes or juvenile diabetes, as it typically develops in childhood or adolescence. In Type 1 diabetes, the immune system mistakenly attacks and destroys the insulin-producing cells in the pancreas, leaving the body unable to produce insulin. Without insulin, glucose (sugar) cannot enter the body's cells for energy, leading to high blood sugar levels. Symptoms of Type 1 diabetes may include frequent urination, excessive thirst, hunger, fatigue, blurred vision, and slow healing of wounds. Treatment typically involves insulin injections or an insulin pump, along with a healthy diet and regular exercise.

Mercuric chloride is a chemical compound that is commonly used in the medical field as an antiseptic and disinfectant. It is also used as a treatment for certain skin conditions, such as acne and psoriasis. However, it is important to note that mercuric chloride is highly toxic and can cause serious health problems if ingested or inhaled. As a result, its use in medical treatments is now limited and is only recommended under the supervision of a qualified healthcare professional.

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disorder that affects multiple organs and systems in the body. It is characterized by the production of autoantibodies that attack healthy cells and tissues, leading to inflammation and damage. The symptoms of SLE can vary widely and may include joint pain and swelling, skin rashes, fatigue, fever, and kidney problems. Other possible symptoms may include chest pain, shortness of breath, headaches, and memory problems. SLE can affect people of all ages and ethnicities, but it is more common in women than in men. There is no known cure for SLE, but treatment can help manage symptoms and prevent complications. Treatment may include medications to reduce inflammation, suppress the immune system, and prevent blood clots. In some cases, hospitalization may be necessary to manage severe symptoms or complications.

Antibodies, Antinuclear (ANA) are proteins produced by the immune system in response to the presence of foreign substances, such as viruses or bacteria. In the medical field, ANA tests are used to detect the presence of these antibodies in the blood. ANA tests are often used to diagnose autoimmune diseases, which are conditions in which the immune system mistakenly attacks healthy cells and tissues in the body. Some autoimmune diseases that can be diagnosed through ANA testing include lupus, rheumatoid arthritis, and Sjogren's syndrome. ANA tests can also be used to monitor the effectiveness of treatment for autoimmune diseases, as well as to detect the presence of certain infections or other medical conditions. However, it's important to note that a positive ANA test does not necessarily mean that a person has an autoimmune disease, as ANA can also be present in healthy individuals.

Autoimmune thyroiditis, also known as Hashimoto's thyroiditis, is a type of thyroiditis that occurs when the immune system attacks the thyroid gland, leading to inflammation and damage to the gland. This condition is characterized by the production of antibodies against the thyroid gland, which can cause the gland to become enlarged and produce less thyroid hormone. Symptoms of autoimmune thyroiditis may include fatigue, weight gain, cold intolerance, constipation, dry skin, and depression. Treatment typically involves hormone replacement therapy with synthetic thyroid hormone to replace the hormone that the damaged thyroid gland is no longer producing.

Encephalomyelitis, Autoimmune, Experimental (EAE) is an animal model of multiple sclerosis (MS), a chronic inflammatory autoimmune disorder that affects the central nervous system (CNS). EAE is induced by the administration of myelin antigens, such as myelin basic protein (MBP), to susceptible animals, which triggers an autoimmune response against the myelin sheath that surrounds nerve fibers in the CNS. In EAE, the immune system mistakenly attacks the myelin sheath, leading to inflammation, demyelination, and axonal damage. This results in a range of neurological symptoms, including paralysis, loss of coordination, and cognitive impairment, which are similar to those seen in MS patients. EAE is widely used in research to study the pathogenesis of MS and to test potential treatments for the disease. It is a valuable tool for understanding the complex interplay between the immune system, the nervous system, and the environment that contributes to the development of MS.

Autoimmune diseases of the nervous system are a group of disorders in which the immune system mistakenly attacks healthy cells and tissues in the nervous system. These diseases can affect any part of the nervous system, including the brain, spinal cord, peripheral nerves, and autonomic nervous system. Examples of autoimmune diseases of the nervous system include multiple sclerosis (MS), Guillain-Barré syndrome (GBS), myasthenia gravis (MG), and lupus erythematosus (LE). These diseases can cause a range of symptoms, including muscle weakness, numbness, tingling, pain, difficulty with coordination and balance, vision problems, and cognitive impairment. The exact cause of autoimmune diseases of the nervous system is not fully understood, but it is believed to involve a combination of genetic and environmental factors. Treatment typically involves medications to suppress the immune system and manage symptoms, as well as physical therapy and other supportive care.

Glutamate decarboxylase (GAD) is an enzyme that plays a critical role in the production of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits the activity of neurons in the central nervous system. GABA is involved in a wide range of physiological processes, including muscle relaxation, anxiety reduction, and sleep regulation. In the medical field, GAD is primarily studied in the context of neurological disorders, particularly those that involve an imbalance in GABA levels. For example, GAD deficiency has been implicated in the development of certain forms of epilepsy, while excessive GABA activity has been linked to anxiety disorders and depression. GAD is also a target for drug development in the treatment of these conditions. For example, medications that increase GABA levels in the brain, such as benzodiazepines, are commonly used to treat anxiety and insomnia. Additionally, drugs that target GAD directly, such as GABA agonists or antagonists, are being investigated as potential treatments for a variety of neurological disorders.

Interleukin-17 (IL-17) is a cytokine, a type of signaling molecule, that plays a role in the immune system's response to infection and inflammation. It is produced by certain types of immune cells, including T cells and natural killer T cells, and is involved in the recruitment and activation of other immune cells, such as neutrophils and macrophages, to the site of infection or injury. IL-17 is also involved in the development of autoimmune diseases, such as rheumatoid arthritis and psoriasis, where it contributes to inflammation and tissue damage. In addition, IL-17 has been implicated in the pathogenesis of inflammatory bowel disease, multiple sclerosis, and other inflammatory conditions. In the medical field, IL-17 is a target for the development of new therapies for autoimmune diseases and other inflammatory conditions. Inhibitors of IL-17, such as biologic drugs, have been shown to be effective in reducing inflammation and improving symptoms in patients with these conditions.

Immunoglobulin G (IgG) is a type of protein that is produced by the immune system in response to the presence of foreign substances, such as bacteria, viruses, and toxins. It is the most abundant type of immunoglobulin in the blood and is responsible for the majority of the body's defense against infections. IgG is produced by B cells, which are a type of white blood cell that plays a key role in the immune response. When a B cell encounters a foreign substance, it produces IgG antibodies that can recognize and bind to the substance, marking it for destruction by other immune cells. IgG antibodies can also be transferred from mother to child through the placenta during pregnancy, providing the baby with some protection against infections during the first few months of life. In addition, some vaccines contain IgG antibodies to help stimulate the immune system and provide protection against specific diseases. Overall, IgG is an important component of the immune system and plays a critical role in protecting the body against infections and diseases.

Forkhead transcription factors (Fox proteins) are a family of transcription factors that play important roles in regulating gene expression in various biological processes, including development, metabolism, and cell proliferation. They are characterized by a conserved DNA-binding domain called the forkhead domain, which is responsible for recognizing and binding to specific DNA sequences. Fox proteins are involved in a wide range of diseases, including cancer, diabetes, and neurodegenerative disorders. For example, mutations in FoxA2, a member of the Fox family, have been linked to the development of type 2 diabetes. In cancer, Fox proteins can act as oncogenes or tumor suppressors, depending on the specific gene and the context in which it is expressed. In the medical field, understanding the role of Fox proteins in disease can provide insights into the underlying mechanisms of disease and may lead to the development of new therapeutic strategies. For example, targeting specific Fox proteins with small molecules or other drugs may be a promising approach for treating cancer or other diseases.

Polyendocrinopathies, autoimmune are a group of rare disorders characterized by the presence of multiple autoimmune diseases affecting the endocrine glands. These glands include the thyroid, adrenal, pituitary, and pancreas, among others. In autoimmune polyendocrinopathies, the immune system mistakenly attacks and damages the endocrine glands, leading to hormonal imbalances and various symptoms. The most common type of autoimmune polyendocrinopathy is the autoimmune polyglandular syndrome type 1 (APS-1), which involves the thyroid, adrenal, and pituitary glands. Other types of autoimmune polyendocrinopathies may involve only one or two endocrine glands. The diagnosis of autoimmune polyendocrinopathies typically involves a combination of clinical symptoms, laboratory tests, and imaging studies. Treatment typically involves hormone replacement therapy to replace the hormones that are not being produced by the affected glands, as well as immunosuppressive medications to control the autoimmune response.

In the medical field, "Disease Models, Animal" refers to the use of animals to study and understand human diseases. These models are created by introducing a disease or condition into an animal, either naturally or through experimental manipulation, in order to study its progression, symptoms, and potential treatments. Animal models are used in medical research because they allow scientists to study diseases in a controlled environment and to test potential treatments before they are tested in humans. They can also provide insights into the underlying mechanisms of a disease and help to identify new therapeutic targets. There are many different types of animal models used in medical research, including mice, rats, rabbits, dogs, and monkeys. Each type of animal has its own advantages and disadvantages, and the choice of model depends on the specific disease being studied and the research question being addressed.

Insulin antibodies are proteins that are produced by the immune system in response to insulin, a hormone that regulates blood sugar levels. These antibodies can interfere with the action of insulin, leading to high blood sugar levels (hyperglycemia) and other complications of diabetes. Insulin antibodies can be detected in the blood through laboratory tests, and their presence can be a sign of type 1 diabetes, in which the immune system attacks and destroys the insulin-producing cells in the pancreas. Insulin antibodies can also be present in people with type 2 diabetes, although they are less common in this condition. In some cases, the presence of insulin antibodies can be a sign of an autoimmune disorder, in which the immune system attacks the body's own tissues. Treatment for insulin antibodies may involve medications to suppress the immune system or to increase insulin production, as well as lifestyle changes such as diet and exercise to help manage blood sugar levels.

Lupus vulgaris is a chronic, inflammatory skin condition caused by the fungus Mycobacterium tuberculosis. It is a type of cutaneous tuberculosis, which means that it affects the skin and underlying tissues. The symptoms of lupus vulgaris can vary, but they typically include a single or multiple, raised, red, and scaly patches on the skin. These patches may be itchy, painful, or tender, and they may also crust over and bleed. The affected skin may also become thickened and leathery over time. Lupus vulgaris is usually diagnosed through a combination of physical examination, skin biopsy, and laboratory tests, such as skin culture or polymerase chain reaction (PCR) testing. Treatment typically involves a combination of antibiotics and corticosteroids to reduce inflammation and fight off the infection. In some cases, surgery may be necessary to remove affected tissue.

B-Cell Activating Factor, also known as BAFF, is a protein that plays a critical role in the development and survival of B cells, a type of white blood cell that produces antibodies. BAFF is produced by various cells in the body, including monocytes, macrophages, and dendritic cells, and it binds to specific receptors on the surface of B cells. BAFF promotes the survival and differentiation of B cells, as well as their ability to produce antibodies. It also plays a role in the development of germinal centers, which are structures in lymph nodes where B cells undergo affinity maturation and class switching to produce high-affinity antibodies. In the medical field, BAFF is important for understanding the pathogenesis of various autoimmune diseases, such as lupus and rheumatoid arthritis, where B cells play a central role. In these conditions, increased levels of BAFF have been associated with the development of autoantibodies and inflammation. As a result, BAFF has become a target for the development of new therapies for autoimmune diseases.

Protein Tyrosine Phosphatase, Non-Receptor Type 22 (PTPN22) is a protein that plays a role in regulating the immune system. It is encoded by the PTPN22 gene and is expressed in various immune cells, including T cells, B cells, and macrophages. PTPN22 is a type of protein tyrosine phosphatase, which is an enzyme that removes phosphate groups from tyrosine residues on other proteins. This process can activate or deactivate the proteins, depending on the context. In the case of PTPN22, it is thought to play a role in regulating the activity of T cells, which are a type of immune cell that plays a central role in the immune response. Mutations in the PTPN22 gene have been associated with an increased risk of several autoimmune diseases, including rheumatoid arthritis, type 1 diabetes, and systemic lupus erythematosus. These mutations are thought to alter the function of PTPN22, leading to dysregulation of the immune system and an increased risk of autoimmune disease.

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis, is an autoimmune disorder that affects the thyroid gland. It is characterized by the production of antibodies that attack and damage the thyroid gland, leading to inflammation and a decrease in the production of thyroid hormones. The symptoms of Hashimoto's thyroiditis can vary widely and may include fatigue, weight gain, cold intolerance, constipation, dry skin, hair loss, depression, and muscle weakness. In some cases, the thyroid gland may become enlarged, a condition known as goiter. Hashimoto's thyroiditis is diagnosed through blood tests that measure thyroid hormone levels and the presence of thyroid antibodies in the blood. Treatment typically involves hormone replacement therapy with synthetic thyroid hormones to replace the hormones that the damaged thyroid gland is no longer producing. In some cases, surgery may be necessary to remove a portion of the thyroid gland or to remove a goiter that is causing symptoms or compressing nearby structures.

Receptors, Antigen, T-Cell are a type of immune cell receptors found on the surface of T cells in the immune system. These receptors are responsible for recognizing and binding to specific antigens, which are foreign substances or molecules that trigger an immune response. T-cell receptors (TCRs) are a type of antigen receptor that recognizes and binds to specific antigens presented on the surface of infected or abnormal cells by major histocompatibility complex (MHC) molecules. TCRs are highly specific and can recognize a wide variety of antigens, including viruses, bacteria, and cancer cells. Once a TCR recognizes an antigen, it sends a signal to the T cell to become activated and initiate an immune response. Activated T cells can then divide and differentiate into different types of effector cells, such as cytotoxic T cells that can directly kill infected or abnormal cells, or helper T cells that can stimulate other immune cells to mount a more robust response. Overall, T-cell receptors play a critical role in the immune system's ability to recognize and respond to foreign antigens, and are an important target for the development of vaccines and immunotherapies.

Vitiligo is a chronic skin disorder characterized by the loss of pigmentation in patches on the skin, hair, and mucous membranes. The patches of depigmented skin are lighter in color than the surrounding skin and may be white, pink, or light brown. Vitiligo is caused by the destruction of melanocytes, the cells responsible for producing melanin, the pigment that gives skin its color. The exact cause of vitiligo is not known, but it is believed to be an autoimmune disorder in which the body's immune system attacks and destroys its own melanocytes. Vitiligo can affect people of all ages, races, and ethnicities, and it can occur anywhere on the body. While vitiligo does not cause any physical harm, it can cause emotional distress and social problems for some people. Treatment options for vitiligo include topical medications, light therapy, and surgery.

Cytokines are small proteins that are produced by various cells of the immune system, including white blood cells, macrophages, and dendritic cells. They play a crucial role in regulating immune responses and inflammation, and are involved in a wide range of physiological processes, including cell growth, differentiation, and apoptosis. Cytokines can be classified into different groups based on their function, including pro-inflammatory cytokines, anti-inflammatory cytokines, and regulatory cytokines. Pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1), promote inflammation and recruit immune cells to the site of infection or injury. Anti-inflammatory cytokines, such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta), help to dampen the immune response and prevent excessive inflammation. Regulatory cytokines, such as interleukin-4 (IL-4) and interleukin-13 (IL-13), help to regulate the balance between pro-inflammatory and anti-inflammatory responses. Cytokines play a critical role in many diseases, including autoimmune disorders, cancer, and infectious diseases. They are also important in the development of vaccines and immunotherapies.

Thyroglobulin is a large glycoprotein that is synthesized and secreted by the thyroid gland. It is the precursor protein for thyroid hormones, thyroxine (T4) and triiodothyronine (T3), which are essential for regulating metabolism in the body. In the medical field, thyroglobulin is often used as a diagnostic marker for thyroid cancer. When thyroid cells become cancerous, they continue to produce thyroglobulin even after the gland has been removed. This means that measuring thyroglobulin levels in the blood can help doctors detect and monitor thyroid cancer. Thyroglobulin levels may also be used to monitor the effectiveness of treatment for thyroid cancer. If the cancer is responding well to treatment, the thyroglobulin levels should decrease. If the levels remain high or increase, it may indicate that the cancer has returned or is still present. In addition to its use in thyroid cancer diagnosis and monitoring, thyroglobulin is also used as a marker for other types of cancer, such as ovarian cancer and breast cancer.

CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) is a protein found on the surface of certain immune cells, including T cells and B cells. It plays a role in regulating the immune response and preventing autoimmune diseases. In the context of the medical field, the CTLA-4 antigen is often studied in the context of cancer immunotherapy. Cancer cells can sometimes evade the immune system by expressing molecules that inhibit the activity of T cells. One such molecule is CTLA-4, which can bind to a protein on the surface of T cells called CD80 or CD86, effectively turning off the T cell's ability to attack cancer cells. Immunotherapies that target CTLA-4 have been developed to help the immune system recognize and attack cancer cells. These therapies work by blocking the interaction between CTLA-4 and CD80/CD86, allowing T cells to mount a stronger immune response against cancer cells. While these therapies have shown promise in some types of cancer, they can also cause side effects such as autoimmune reactions.

Iodide Peroxidase (also known as Thyroid Peroxidase) is an enzyme that plays a critical role in the production of thyroid hormones in the thyroid gland. It catalyzes the oxidation of iodide ions to form iodine, which is then incorporated into thyroglobulin, a large protein produced by thyroid cells. The iodinated thyroglobulin is then broken down into smaller thyroid hormones, thyroxine (T4) and triiodothyronine (T3), which are essential for regulating metabolism in the body. In the medical field, the measurement of thyroid peroxidase antibodies (TPOAb) is often used as a diagnostic tool for autoimmune thyroid diseases such as Hashimoto's thyroiditis and Graves' disease. In these conditions, the immune system mistakenly attacks the thyroid gland, leading to inflammation and damage to the gland's ability to produce thyroid hormones. The presence of TPOAb in the blood can indicate an autoimmune response and help guide treatment decisions.

Lymphopenia is a medical condition characterized by a reduced number of lymphocytes, a type of white blood cell, in the blood. Lymphocytes are an important part of the immune system and play a crucial role in fighting infections and diseases. Lymphopenia can be caused by a variety of factors, including infections, autoimmune disorders, certain medications, and cancer treatments. It can also be a sign of an underlying medical condition, such as HIV/AIDS, leukemia, or lymphoma. Symptoms of lymphopenia may include fatigue, weakness, fever, and an increased susceptibility to infections. Treatment for lymphopenia depends on the underlying cause and may include medications, lifestyle changes, or medical procedures.

Multiple Sclerosis (MS) is a chronic autoimmune disorder that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. In MS, the immune system attacks and damages the protective covering (myelin) that surrounds nerve fibers in the CNS, leading to inflammation, scarring (sclerosis), and loss of nerve function. The symptoms of MS can vary widely and may include: - Fatigue - Muscle weakness - Numbness or tingling in the limbs - Blurred vision - Difficulty with coordination and balance - Difficulty speaking or understanding speech - Seizures - Depression and anxiety MS can be diagnosed through a combination of physical exams, medical history, and imaging tests such as magnetic resonance imaging (MRI). There is currently no cure for MS, but treatments are available to manage symptoms and slow the progression of the disease.

Thyroid diseases refer to a group of disorders that affect the thyroid gland, a small endocrine gland located in the neck that produces hormones that regulate metabolism. The thyroid gland produces two main hormones: thyroxine (T4) and triiodothyronine (T3), which are essential for regulating the body's metabolism, growth, and development. There are several types of thyroid diseases, including: 1. Hypothyroidism: This is a condition in which the thyroid gland does not produce enough thyroid hormones. Symptoms of hypothyroidism include fatigue, weight gain, cold intolerance, dry skin, and depression. 2. Hyperthyroidism: This is a condition in which the thyroid gland produces too much thyroid hormone. Symptoms of hyperthyroidism include weight loss, rapid heartbeat, anxiety, and tremors. 3. Thyroid nodules: These are small growths on the thyroid gland that can be benign or malignant. 4. Thyroiditis: This is an inflammation of the thyroid gland that can cause symptoms such as pain, swelling, and difficulty swallowing. 5. Thyroid cancer: This is a rare type of cancer that affects the thyroid gland. Symptoms of thyroid cancer may include a lump in the neck, difficulty swallowing, and hoarseness. Thyroid diseases can be diagnosed through blood tests, imaging studies, and physical examination. Treatment options for thyroid diseases depend on the specific condition and may include medication, surgery, or radiation therapy.

HLA-DQ antigens are a group of proteins found on the surface of cells in the human body. They are part of the human leukocyte antigen (HLA) system, which plays a critical role in the immune system's ability to recognize and respond to foreign substances, such as viruses and bacteria. HLA-DQ antigens are particularly important in the immune response to certain types of infections, including those caused by viruses such as HIV and hepatitis C. They also play a role in the development of certain autoimmune diseases, such as celiac disease and type 1 diabetes. HLA-DQ antigens are classified into two main groups: HLA-DQ1 and HLA-DQ2. These groups are further divided into several subtypes, each with a unique combination of amino acids in their protein structure. The specific HLA-DQ antigens present on the surface of a person's cells can affect their susceptibility to certain diseases and their response to certain treatments.

Inflammation is a complex biological response of the body to harmful stimuli, such as pathogens, damaged cells, or irritants. It is a protective mechanism that helps to eliminate the cause of injury, remove damaged tissue, and initiate the healing process. Inflammation involves the activation of immune cells, such as white blood cells, and the release of chemical mediators, such as cytokines and prostaglandins. This leads to the characteristic signs and symptoms of inflammation, including redness, heat, swelling, pain, and loss of function. Inflammation can be acute or chronic. Acute inflammation is a short-term response that lasts for a few days to a few weeks and is usually beneficial. Chronic inflammation, on the other hand, is a prolonged response that lasts for months or years and can be harmful if it persists. Chronic inflammation is associated with many diseases, including cancer, cardiovascular disease, and autoimmune disorders.

Interferon-gamma (IFN-γ) is a type of cytokine, which is a signaling molecule that plays a crucial role in the immune system. It is produced by various immune cells, including T cells, natural killer cells, and macrophages, in response to viral or bacterial infections, as well as in response to certain types of cancer. IFN-γ has a wide range of effects on the immune system, including the activation of macrophages and other immune cells, the inhibition of viral replication, and the promotion of T cell differentiation and proliferation. It also plays a role in the regulation of the immune response, helping to prevent excessive inflammation and tissue damage. In the medical field, IFN-γ is used as a therapeutic agent in the treatment of certain types of cancer, such as Hodgkin's lymphoma and multiple myeloma. It is also being studied as a potential treatment for other conditions, such as autoimmune diseases and viral infections.

Genetic predisposition to disease refers to the tendency of an individual to develop a particular disease or condition due to their genetic makeup. It means that certain genes or combinations of genes increase the risk of developing a particular disease or condition. Genetic predisposition to disease is not the same as having the disease itself. It simply means that an individual has a higher likelihood of developing the disease compared to someone without the same genetic predisposition. Genetic predisposition to disease can be inherited from parents or can occur due to spontaneous mutations in genes. Some examples of genetic predisposition to disease include hereditary breast and ovarian cancer, Huntington's disease, cystic fibrosis, and sickle cell anemia. Understanding genetic predisposition to disease is important in medical practice because it can help identify individuals who are at high risk of developing a particular disease and allow for early intervention and prevention strategies to be implemented.

HLA-DQ beta-Chains are a type of protein found on the surface of cells in the human body. They are part of the major histocompatibility complex (MHC) and play a role in the immune system's ability to recognize and respond to foreign substances, such as viruses and bacteria. There are several different types of HLA-DQ beta-Chains, which are encoded by different genes on chromosome 6. These genes are highly polymorphic, meaning that there are many different variations of the HLA-DQ beta-Chains that can be found in the human population. This diversity allows the immune system to recognize a wide range of different foreign substances. HLA-DQ beta-Chains are particularly important in the immune system's response to food antigens. They help to present these antigens to T cells, which are a type of immune cell that plays a key role in the immune response. This process is known as antigen presentation and is an important step in the development of food allergies and other immune-mediated disorders. In addition to their role in the immune system, HLA-DQ beta-Chains have also been implicated in the development of certain autoimmune diseases, such as celiac disease and type 1 diabetes. In these conditions, the immune system mistakenly attacks the body's own tissues, leading to inflammation and damage.

Splenomegaly is a medical condition characterized by an enlargement of the spleen, which is a vital organ in the body that plays a crucial role in the immune system. The spleen is responsible for filtering blood, removing old or damaged red blood cells, and producing white blood cells that help fight infections. Splenomegaly can be caused by a variety of factors, including infections, autoimmune disorders, blood disorders, and certain types of cancer. In some cases, the cause of splenomegaly may be unknown. Symptoms of splenomegaly may include abdominal pain, discomfort, and fullness, as well as fatigue, weakness, and anemia. In severe cases, splenomegaly can lead to complications such as bleeding, infection, and organ failure. Diagnosis of splenomegaly typically involves a physical examination, blood tests, imaging studies such as ultrasound or CT scans, and in some cases, a biopsy of the spleen. Treatment of splenomegaly depends on the underlying cause and may include medications, surgery, or other therapies.

Collagen Type V is a protein that is found in the extracellular matrix of connective tissues in the human body. It is a component of the fibrillar collagen network, which provides strength and support to tissues such as skin, tendons, ligaments, and bone. Collagen Type V is a heterotrimeric protein, meaning that it is composed of three different chains of collagen, called alpha chains. The three alpha chains of collagen Type V are called alpha 1(V), alpha 2(V), and alpha 3(V). Collagen Type V is known for its unique triple helical structure, which is formed by the winding of the three alpha chains around each other. This structure gives collagen its strength and flexibility. In addition to its structural role in connective tissues, collagen Type V has also been implicated in a number of biological processes, including cell signaling, tissue development, and wound healing. It is also involved in the regulation of blood vessel formation and the development of blood clots. Research has suggested that collagen Type V may play a role in the development of certain diseases, including osteoporosis, atherosclerosis, and certain types of cancer. As a result, there is ongoing interest in understanding the function of collagen Type V and developing therapies that target this protein.

Graves' disease is an autoimmune disorder that affects the thyroid gland, a small gland located in the neck that produces hormones that regulate metabolism. In Graves' disease, the immune system mistakenly attacks the thyroid gland, causing it to produce excessive amounts of thyroid hormones, a condition known as hyperthyroidism. The symptoms of Graves' disease can vary widely and may include weight loss, rapid or irregular heartbeat, anxiety, tremors, heat intolerance, sweating, and bulging eyes (Graves' ophthalmopathy). The disease can also cause swelling of the thyroid gland, known as a goiter. Graves' disease is typically treated with medications that help to reduce the production of thyroid hormones, such as methimazole or propylthiouracil. In some cases, surgery or radioactive iodine therapy may be necessary to remove the overactive thyroid gland or destroy the gland's ability to produce hormones.

Lupus nephritis is a type of kidney inflammation that occurs as a complication of systemic lupus erythematosus (SLE), an autoimmune disorder in which the body's immune system attacks healthy cells and tissues. Lupus nephritis is characterized by inflammation and damage to the glomeruli, which are the tiny blood vessels in the kidneys responsible for filtering waste products from the blood. This can lead to a range of symptoms, including protein in the urine, swelling in the legs and feet, high blood pressure, and decreased kidney function. Treatment for lupus nephritis typically involves a combination of medications to reduce inflammation and control blood pressure, as well as lifestyle changes to promote overall health and well-being.

Rheumatoid arthritis (RA) is a chronic autoimmune disorder that primarily affects the joints. It is characterized by inflammation and damage to the lining of the joint capsule, which leads to pain, stiffness, and reduced range of motion. RA can also affect other organs, such as the lungs, heart, and eyes. RA is a systemic disease, meaning that it affects the entire body, not just the joints. It is an inflammatory disease, meaning that it is caused by the immune system attacking healthy cells and tissues in the body. RA is a progressive disease, meaning that it can worsen over time if left untreated. However, with proper treatment, it is possible to manage the symptoms and slow down the progression of the disease. The exact cause of RA is not fully understood, but it is believed to be a combination of genetic and environmental factors. Risk factors for RA include being female, having a family history of the disease, and smoking.

Myelin-Oligodendrocyte Glycoprotein (MOG) is a protein that is expressed on the surface of oligodendrocytes, which are a type of glial cell that produce myelin in the central nervous system (CNS). Myelin is a fatty substance that surrounds and insulates nerve fibers, allowing them to transmit electrical signals more efficiently. MOG is a type of autoantigen, which means that it can trigger an immune response in the body. In some cases, this immune response can lead to the destruction of myelin and the formation of lesions in the CNS, a condition known as multiple sclerosis (MS). MOG-related disorders are a group of conditions that are characterized by the production of antibodies against MOG and the development of inflammation and demyelination in the CNS. MOG-related disorders can present with a range of symptoms, including weakness, numbness, tingling, and vision problems. Some people may also experience cognitive and emotional changes, as well as fatigue and difficulty walking. Treatment for MOG-related disorders typically involves the use of immunosuppressive medications to reduce inflammation and prevent further damage to the CNS.

Interleukin-2 receptor alpha subunit (IL-2Rα) is a protein that plays a crucial role in the immune system. It is a component of the interleukin-2 receptor complex, which is found on the surface of immune cells such as T cells, natural killer cells, and macrophages. The IL-2Rα subunit is a transmembrane protein that consists of an extracellular domain, a single transmembrane domain, and an intracellular domain. When interleukin-2 (IL-2), a cytokine produced by activated T cells, binds to the IL-2Rα subunit, it triggers a signaling cascade that leads to the activation and proliferation of immune cells. In the medical field, the IL-2Rα subunit is often studied in the context of autoimmune diseases, cancer, and infectious diseases. For example, in some autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis, the overexpression of IL-2Rα on immune cells can contribute to inflammation and tissue damage. In cancer, the overexpression of IL-2Rα on tumor cells can make them more susceptible to immune attack by T cells. In infectious diseases, the IL-2Rα subunit can play a role in the activation of immune cells that are involved in the immune response to the pathogen.

Sjogren's Syndrome is a chronic autoimmune disorder that affects the exocrine glands, particularly the salivary and lacrimal glands. It is characterized by dryness of the mouth and eyes, as well as other symptoms such as fatigue, joint pain, and dry skin. The exact cause of Sjogren's Syndrome is not known, but it is believed to be triggered by a combination of genetic and environmental factors. The condition can range from mild to severe, and treatment typically involves managing symptoms and addressing any complications that arise.

Hypergammaglobulinemia is a medical condition characterized by an abnormally high level of gamma globulins, a type of protein found in the blood. Gamma globulins are a component of the immune system and are produced by specialized white blood cells called plasma cells. Hypergammaglobulinemia can be caused by a variety of factors, including infections, autoimmune disorders, certain types of cancer, and genetic disorders. In some cases, the cause of hypergammaglobulinemia may not be identified. Symptoms of hypergammaglobulinemia may include fatigue, weakness, joint pain, and swelling. In some cases, hypergammaglobulinemia may be asymptomatic and be discovered through routine blood tests. Treatment for hypergammaglobulinemia depends on the underlying cause. In some cases, no treatment may be necessary if the condition is asymptomatic. However, if hypergammaglobulinemia is caused by an underlying condition, such as an infection or autoimmune disorder, treatment for that condition may be necessary. In some cases, medications may be used to lower the level of gamma globulins in the blood.

Histocompatibility antigens class II are a group of proteins found on the surface of certain cells in the immune system. These proteins play a crucial role in the immune response by presenting foreign substances, such as bacteria or viruses, to immune cells called T cells. The class II antigens are encoded by a group of genes called the major histocompatibility complex (MHC) class II genes. These genes are located on chromosome 6 in humans and are highly polymorphic, meaning that there are many different versions of the genes. This diversity of MHC class II antigens allows the immune system to recognize and respond to a wide variety of foreign substances.

Receptor-like protein tyrosine phosphatases, class 8 (PTPRC8) are a group of proteins that are involved in cell signaling and have been identified as potential therapeutic targets for various diseases. These proteins are characterized by their ability to remove phosphate groups from tyrosine residues on other proteins, which can regulate their activity and function. PTPRC8 proteins are expressed in a variety of tissues and cell types, including immune cells, neurons, and epithelial cells. They have been implicated in a number of biological processes, including cell adhesion, migration, and differentiation, as well as in the regulation of the immune response. In the medical field, PTPRC8 proteins have been studied in the context of various diseases, including cancer, autoimmune disorders, and infectious diseases. For example, some studies have suggested that PTPRC8 may play a role in the development and progression of certain types of cancer, such as breast cancer and leukemia. Other research has suggested that PTPRC8 may be involved in the regulation of the immune response to infections, such as those caused by viruses and bacteria. Overall, PTPRC8 proteins are an important area of research in the medical field, as they have the potential to play a role in the development and treatment of a variety of diseases.

Myelin Basic Protein (MBP) is a protein that is found in the myelin sheath, which is a fatty layer that surrounds and insulates nerve fibers in the central nervous system (CNS). MBP plays a crucial role in the formation and maintenance of the myelin sheath, and it is thought to be involved in the development and progression of several neurological disorders, including multiple sclerosis (MS), neuromyelitis optica (NMO), and some forms of leukodystrophy. In these conditions, the immune system mistakenly attacks the myelin sheath, leading to inflammation and damage to the nerve fibers. MBP is also being studied as a potential biomarker for these disorders, as levels of MBP in the blood or cerebrospinal fluid may be elevated in people with these conditions.

Uveitis is an inflammation of the uvea, which is the middle layer of the eye that includes the iris, ciliary body, and choroid. It can affect one or both eyes and can be caused by a variety of factors, including infections, autoimmune disorders, and certain medications. Symptoms of uveitis may include redness, pain, sensitivity to light, blurred vision, and floaters. If left untreated, uveitis can lead to serious complications, such as glaucoma, cataracts, and vision loss. Treatment for uveitis typically involves the use of corticosteroids and other anti-inflammatory medications, as well as management of any underlying causes of the inflammation.

Thyroiditis is a medical condition characterized by inflammation of the thyroid gland, which is a small gland located in the neck that produces hormones that regulate metabolism. There are several types of thyroiditis, including: 1. Subacute thyroiditis: This is a type of thyroiditis that is caused by a viral infection and is characterized by pain and swelling in the thyroid gland. 2. Hashimoto's thyroiditis: This is an autoimmune disorder in which the immune system attacks the thyroid gland, leading to inflammation and damage to the gland. 3. Postpartum thyroiditis: This is a type of thyroiditis that occurs in women after giving birth and is characterized by inflammation and swelling of the thyroid gland. 4. Thyroiditis associated with Graves' disease: This is a type of thyroiditis that occurs in people with Graves' disease, an autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone. Symptoms of thyroiditis may include pain or tenderness in the neck, swelling of the thyroid gland, fatigue, weight gain or loss, and changes in heart rate or blood pressure. Treatment for thyroiditis depends on the underlying cause and may include medications to manage symptoms or treat the underlying condition, as well as lifestyle changes such as a healthy diet and regular exercise.

Stiff-Person Syndrome (SPS) is a rare autoimmune disorder that affects the nervous system. It is characterized by muscle stiffness and spasms, particularly in the trunk and limbs, which can be triggered by emotional stress or physical stimuli. SPS can also cause a variety of other symptoms, including muscle weakness, fatigue, and joint pain. The stiffness and spasms can be so severe that they can interfere with daily activities and make it difficult to walk or perform other basic tasks. SPS is a lifelong condition, but treatment can help manage symptoms and improve quality of life.

Arthritis, Experimental refers to the study of arthritis using experimental methods, such as animal models or in vitro studies, to better understand the underlying mechanisms of the disease and to develop new treatments. Experimental arthritis is often induced in animals through the use of chemicals or by introducing an infectious agent, such as bacteria or viruses, into the joints. These studies can help researchers identify potential targets for therapy and test the effectiveness of new drugs or other interventions in a controlled setting before they are tested in humans.

Infection is a disease caused by the invasion and multiplication of pathogenic microorganisms, such as bacteria, viruses, fungi, or parasites, in the body. These microorganisms can enter the body through various routes, such as the respiratory system, digestive system, skin, or bloodstream. Infections can cause a wide range of symptoms, depending on the type of microorganism and the affected body. Common symptoms of infections include fever, chills, fatigue, body aches, cough, sore throat, runny nose, diarrhea, vomiting, and skin rashes. Infections can be treated with antibiotics, antiviral drugs, antifungal medications, or antiparasitic drugs, depending on the type of microorganism causing the infection. In some cases, supportive care, such as rest, fluids, and pain relief, may be necessary to help the body fight off the infection. Preventing infections is also important, and can be achieved through good hygiene practices, such as washing hands regularly, covering the mouth and nose when coughing or sneezing, and avoiding close contact with sick individuals. Vaccines can also be used to prevent certain types of infections, such as influenza, measles, and pneumonia.

Monoclonal antibodies (mAbs) are laboratory-made proteins that can mimic the immune system's ability to fight off harmful pathogens, such as viruses and bacteria. They are produced by genetically engineering cells to produce large quantities of a single type of antibody, which is specific to a particular antigen (a molecule that triggers an immune response). In the medical field, monoclonal antibodies are used to treat a variety of conditions, including cancer, autoimmune diseases, and infectious diseases. They can be administered intravenously, intramuscularly, or subcutaneously, depending on the condition being treated. Monoclonal antibodies work by binding to specific antigens on the surface of cells or pathogens, marking them for destruction by the immune system. They can also block the activity of specific molecules involved in disease processes, such as enzymes or receptors. Overall, monoclonal antibodies have revolutionized the treatment of many diseases, offering targeted and effective therapies with fewer side effects than traditional treatments.

Immunoglobulin M (IgM) is a type of antibody that is produced by B cells in response to an infection or foreign substance. It is the first antibody to be produced during an immune response and is present in the blood and other body fluids in relatively low concentrations. IgM antibodies are large, Y-shaped molecules that can bind to multiple antigens at once, making them highly effective at neutralizing pathogens and marking them for destruction by other immune cells. They are also able to activate the complement system, a series of proteins that can directly destroy pathogens or mark them for destruction by immune cells. IgM antibodies are often used as a diagnostic tool in medical testing, as they are typically the first antibodies to be produced in response to a new infection. They can also be used to monitor the effectiveness of vaccines and to detect the presence of certain diseases, such as viral or bacterial infections, autoimmune disorders, and certain types of cancer.

Lymphoproliferative disorders are a group of conditions characterized by the abnormal growth and proliferation of lymphocytes, a type of white blood cell that plays a crucial role in the immune system. These disorders can affect any part of the lymphatic system, including the lymph nodes, spleen, bone marrow, and thymus. Lymphoproliferative disorders can be classified into two main categories: Hodgkin lymphoma and non-Hodgkin lymphoma. Hodgkin lymphoma is a type of cancer that affects the lymphatic system, while non-Hodgkin lymphoma is a more general term that encompasses a wide range of lymphatic system disorders, including lymphoma, leukemia, and myeloma. Lymphoproliferative disorders can be caused by a variety of factors, including viral infections, genetic mutations, and exposure to certain chemicals or radiation. Symptoms of these disorders can vary widely depending on the specific type and location of the affected lymphatic tissue, but may include swelling of the lymph nodes, fatigue, fever, night sweats, and weight loss. Treatment for lymphoproliferative disorders typically involves a combination of chemotherapy, radiation therapy, and/or immunotherapy, depending on the specific type and stage of the disorder. In some cases, a stem cell transplant may also be necessary. The prognosis for lymphoproliferative disorders varies depending on the specific type and stage of the disorder, as well as the age and overall health of the patient.

Lymphatic diseases refer to a group of disorders that affect the lymphatic system, which is a network of vessels, tissues, and organs that help to transport lymph fluid throughout the body. The lymphatic system plays a crucial role in the immune system, as it helps to filter out harmful substances and transport white blood cells to areas of the body where they are needed to fight infections. Lymphatic diseases can affect any part of the lymphatic system, including the lymph nodes, lymph vessels, and the spleen. Some common examples of lymphatic diseases include: 1. Lymphedema: A condition in which the lymphatic system is unable to drain lymph fluid properly, leading to swelling in the affected area. 2. Lymphoma: A type of cancer that affects the lymphatic system, causing the growth of abnormal lymphocytes (white blood cells) in the lymph nodes and other tissues. 3. Castleman's disease: A rare disorder characterized by the abnormal growth of lymph nodes, which can cause symptoms such as fever, weight loss, and fatigue. 4. Lymphatic filariasis: A parasitic infection that affects the lymphatic system, causing swelling in the legs and other areas of the body. 5. Primary Sjogren's syndrome: An autoimmune disorder that affects the glands that produce saliva and tears, leading to dryness and inflammation in the eyes and mouth. Treatment for lymphatic diseases depends on the specific condition and its severity. In some cases, medications or lifestyle changes may be sufficient to manage symptoms. In more severe cases, surgery or other medical interventions may be necessary.

Receptors, Interleukin-2 (IL-2) are proteins found on the surface of certain immune cells, such as T cells and natural killer cells. These receptors are responsible for binding to the cytokine Interleukin-2 (IL-2), which is produced by activated T cells and other immune cells. When IL-2 binds to its receptor, it triggers a signaling cascade within the cell that promotes the growth, survival, and activation of immune cells. This process is important for the proper functioning of the immune system and the body's ability to fight off infections and diseases.

Interleukin-10 (IL-10) is a cytokine, which is a type of signaling molecule that plays a role in regulating the immune system. It is produced by various immune cells, including macrophages, dendritic cells, and T cells, in response to infection or inflammation. IL-10 has anti-inflammatory properties and helps to suppress the immune response, which can be beneficial in preventing excessive inflammation and tissue damage. It also has immunosuppressive effects, which can help to prevent autoimmune diseases and transplant rejection. In the medical field, IL-10 is being studied for its potential therapeutic applications in a variety of conditions, including inflammatory diseases, autoimmune diseases, and cancer. For example, IL-10 has been shown to be effective in reducing inflammation and improving symptoms in patients with rheumatoid arthritis, Crohn's disease, and other inflammatory conditions. It is also being investigated as a potential treatment for cancer, as it may help to suppress the immune response that allows cancer cells to evade detection and destruction by the immune system.

Immunologic Deficiency Syndromes (IDS) are a group of disorders that affect the immune system, which is the body's natural defense against infections and diseases. In individuals with IDS, the immune system is either absent or not functioning properly, making them more susceptible to infections and diseases that would not normally pose a threat to healthy individuals. IDS can be classified into primary and secondary immunodeficiencies. Primary immunodeficiencies are genetic disorders that affect the immune system from birth or early childhood, while secondary immunodeficiencies are acquired later in life due to other medical conditions or treatments such as chemotherapy or radiation therapy. Some common examples of IDS include: * Severe Combined Immunodeficiency (SCID): a rare genetic disorder in which the immune system is severely impaired, making individuals highly susceptible to infections. * Common Variable Immunodeficiency (CVID): a primary immunodeficiency characterized by low levels of antibodies in the blood, making individuals prone to recurrent infections. * Wiskott-Aldrich Syndrome (WAS): a primary immunodeficiency characterized by low levels of platelets and recurrent infections. * X-linked Agammaglobulinemia (XLA): a primary immunodeficiency characterized by low levels of antibodies and recurrent infections. Treatment for IDS typically involves immunoglobulin replacement therapy, antibiotics, and other supportive care to manage infections and complications. In some cases, bone marrow transplantation or gene therapy may be considered as a potential cure.

Interleukin-2 (IL-2) is a cytokine, a type of signaling molecule that plays a crucial role in the immune system. It is produced by activated T cells, a type of white blood cell that plays a central role in the body's defense against infection and disease. IL-2 has several important functions in the immune system. It promotes the growth and differentiation of T cells, which helps to increase the number of immune cells available to fight infection. It also stimulates the production of other cytokines, which can help to amplify the immune response. IL-2 is used in the treatment of certain types of cancer, such as melanoma and kidney cancer. It works by stimulating the immune system to attack cancer cells. It is typically given as an injection or infusion, and can cause side effects such as fever, chills, and flu-like symptoms. In addition to its use in cancer treatment, IL-2 has also been studied for its potential role in treating other conditions, such as autoimmune diseases and viral infections.

In the medical field, a peptide fragment refers to a short chain of amino acids that are derived from a larger peptide or protein molecule. Peptide fragments can be generated through various techniques, such as enzymatic digestion or chemical cleavage, and are often used in diagnostic and therapeutic applications. Peptide fragments can be used as biomarkers for various diseases, as they may be present in the body at elevated levels in response to specific conditions. For example, certain peptide fragments have been identified as potential biomarkers for cancer, neurodegenerative diseases, and cardiovascular disease. In addition, peptide fragments can be used as therapeutic agents themselves. For example, some peptide fragments have been shown to have anti-inflammatory or anti-cancer properties, and are being investigated as potential treatments for various diseases. Overall, peptide fragments play an important role in the medical field, both as diagnostic tools and as potential therapeutic agents.

Interleukin-23 (IL-23) is a cytokine that plays a critical role in the regulation of the immune system. It is produced by immune cells called dendritic cells and macrophages, and it acts on other immune cells, such as T cells and B cells, to stimulate their activity. IL-23 is involved in the development and maintenance of autoimmune diseases, such as psoriasis and Crohn's disease, as well as in the regulation of the immune response to infections. It promotes the differentiation and proliferation of T cells that produce the cytokine interleukin-17 (IL-17), which is involved in the recruitment of immune cells to sites of inflammation. In the medical field, IL-23 is being studied as a potential target for the treatment of autoimmune diseases. In particular, monoclonal antibodies that block the action of IL-23 are being developed as therapies for psoriasis and Crohn's disease. These drugs have shown promise in clinical trials, and they are being evaluated for their safety and efficacy in treating these conditions.

HLA-DR antigens are a group of proteins that are expressed on the surface of cells of the immune system. They play a crucial role in the recognition and presentation of antigens to T cells, which is a key step in the immune response. HLA-DR antigens are encoded by the HLA-DR gene, which is located on chromosome 6. There are many different HLA-DR antigens, each with a unique sequence of amino acids that determines its specificity for different antigens. HLA-DR antigens are also known as human leukocyte antigen (HLA) DR antigens or major histocompatibility complex (MHC) class II DR antigens.

Arthritis is a medical condition that involves inflammation of one or more joints in the body. It can cause pain, stiffness, and swelling in the affected joints, and can limit mobility and range of motion. There are many different types of arthritis, including osteoarthritis, rheumatoid arthritis, psoriatic arthritis, and lupus arthritis, among others. Arthritis can affect people of all ages, but it is most common in older adults. Treatment for arthritis typically involves a combination of medications, physical therapy, and lifestyle changes, such as exercise and a healthy diet.

Interleukins are a group of signaling proteins that are produced by various cells of the immune system, including white blood cells, and play a crucial role in regulating immune responses. They are also involved in a wide range of other physiological processes, such as cell growth, differentiation, and apoptosis (programmed cell death). Interleukins are classified into different groups based on their structure and function. Some of the most well-known interleukins include interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), and interleukin-12 (IL-12). Interleukins can act locally within tissues or be transported through the bloodstream to other parts of the body. They can also bind to specific receptors on the surface of target cells, triggering a signaling cascade that leads to changes in gene expression and cellular function. In the medical field, interleukins are often used as therapeutic agents to treat a variety of conditions, including autoimmune diseases, cancer, and infections. They can also be used as diagnostic tools to help identify and monitor certain diseases.

Receptors, Antigen, B-Cell are a type of immune cell receptors found on the surface of B cells in the immune system. These receptors are responsible for recognizing and binding to specific antigens, which are foreign substances such as viruses, bacteria, or other pathogens. When a B cell encounters an antigen that matches its receptor, it becomes activated and begins to produce antibodies, which are proteins that can recognize and neutralize the specific antigen. The production of antibodies by B cells is a key part of the adaptive immune response, which helps the body to defend against infections and other harmful substances.

Myocarditis is an inflammation of the heart muscle (myocardium) that can be caused by a viral or bacterial infection, autoimmune disorders, or other factors. It can lead to swelling and damage to the heart muscle, which can affect its ability to pump blood effectively. Symptoms of myocarditis can include chest pain, shortness of breath, fatigue, and an irregular heartbeat. Treatment for myocarditis depends on the underlying cause and may include medications, rest, and lifestyle changes. In severe cases, hospitalization and supportive care may be necessary. Myocarditis can be a serious condition and can lead to complications such as heart failure, arrhythmias, and sudden cardiac death.

Disease susceptibility refers to an individual's increased risk of developing a particular disease or condition due to genetic, environmental, or lifestyle factors. Susceptibility to a disease is not the same as having the disease itself, but rather an increased likelihood of developing it compared to someone who is not susceptible. Genetic factors play a significant role in disease susceptibility. Certain genetic mutations or variations can increase an individual's risk of developing certain diseases, such as breast cancer, diabetes, or heart disease. Environmental factors, such as exposure to toxins or pollutants, can also increase an individual's susceptibility to certain diseases. Lifestyle factors, such as diet, exercise, and smoking, can also impact disease susceptibility. For example, a diet high in saturated fats and sugar can increase an individual's risk of developing heart disease, while regular exercise can reduce the risk. Understanding an individual's disease susceptibility can help healthcare providers develop personalized prevention and treatment plans to reduce the risk of developing certain diseases or to manage existing conditions more effectively.

Mercury is a toxic heavy metal that has been used in various medical applications throughout history. In the modern medical field, mercury is no longer used for most medical purposes due to its harmful effects on human health. However, there are still some medical applications where mercury is used, although its use is highly regulated and restricted. One such application is in the treatment of certain types of syphilis, where mercury-based medications called "mercurials" were once used. These medications are no longer used due to their severe side effects and the availability of safer alternatives. Mercury can also be found in some medical devices, such as thermometers and blood pressure cuffs, although the use of mercury in these devices is also being phased out due to concerns about its environmental impact and potential health risks. Overall, while mercury has had some medical applications in the past, its use is now highly restricted and regulated due to its toxic nature.

Anemia, Hemolytic, Autoimmune is a type of anemia that occurs when the immune system attacks and destroys red blood cells, leading to their premature destruction or breakdown. This type of anemia is also known as autoimmune hemolytic anemia (AIHA). In AIHA, the immune system produces antibodies that target red blood cells, causing them to be destroyed by the spleen or liver. This leads to a decrease in the number of red blood cells in the body, which can cause symptoms such as fatigue, weakness, shortness of breath, and pale skin. There are several types of AIHA, including warm antibody AIHA, cold antibody AIHA, and paroxysmal cold hemoglobinuria. Treatment for AIHA typically involves medications to suppress the immune system, such as corticosteroids or immunosuppressive drugs, as well as blood transfusions in severe cases.

Receptors, Antigen, T-Cell, alpha-beta are a type of immune cell receptor found on the surface of T-cells in the human body. These receptors are responsible for recognizing and binding to specific antigens, which are foreign substances that trigger an immune response. The alpha-beta receptors are a type of T-cell receptor that recognizes antigens presented by major histocompatibility complex (MHC) molecules on the surface of infected or cancerous cells. When the alpha-beta receptors bind to the antigen-MHC complex, it triggers a series of events that lead to the activation and proliferation of the T-cell, which then mounts an immune response against the infected or cancerous cells.

Immunoglobulins, also known as antibodies, are proteins produced by the immune system in response to the presence of foreign substances, such as viruses, bacteria, and toxins. They are Y-shaped molecules that recognize and bind to specific antigens, which are molecules found on the surface of pathogens. There are five main classes of immunoglobulins: IgG, IgA, IgM, IgD, and IgE. Each class has a unique structure and function, and they are produced by different types of immune cells in response to different types of pathogens. Immunoglobulins play a critical role in the immune response by neutralizing pathogens, marking them for destruction by other immune cells, and activating the complement system, which helps to destroy pathogens. They are also used in medical treatments, such as immunoglobulin replacement therapy for patients with primary immunodeficiencies, and in the development of vaccines and monoclonal antibodies for the treatment of various diseases.

Antibodies, also known as immunoglobulins, are proteins produced by the immune system in response to the presence of foreign substances, such as viruses, bacteria, and other pathogens. Antibodies are designed to recognize and bind to specific molecules on the surface of these foreign substances, marking them for destruction by other immune cells. There are five main classes of antibodies: IgG, IgA, IgM, IgD, and IgE. Each class of antibody has a unique structure and function, and they are produced by different types of immune cells in response to different types of pathogens. Antibodies play a critical role in the immune response, helping to protect the body against infection and disease. They can neutralize pathogens by binding to them and preventing them from entering cells, or they can mark them for destruction by other immune cells. In some cases, antibodies can also help to stimulate the immune response by activating immune cells or by recruiting other immune cells to the site of infection. Antibodies are often used in medical treatments, such as in the development of vaccines, where they are used to stimulate the immune system to produce a response to a specific pathogen. They are also used in diagnostic tests to detect the presence of specific pathogens or to monitor the immune response to a particular treatment.

An antigen-antibody complex is a type of immune complex that forms when an antigen (a foreign substance that triggers an immune response) binds to an antibody (a protein produced by the immune system to recognize and neutralize antigens). When an antigen enters the body, it is recognized by specific antibodies that bind to it, forming an antigen-antibody complex. This complex can then be targeted by other immune cells, such as phagocytes, which engulf and destroy the complex. Antigen-antibody complexes can also deposit in tissues, leading to inflammation and damage. This can occur in conditions such as immune complex-mediated diseases, where the immune system mistakenly attacks healthy tissues that have been coated with antigens and antibodies. Overall, the formation of antigen-antibody complexes is a normal part of the immune response, but when it becomes dysregulated, it can lead to a variety of medical conditions.

Glomerulonephritis is a type of kidney disease that involves inflammation of the glomeruli, which are tiny blood vessels in the kidneys responsible for filtering waste products from the blood. This inflammation can cause damage to the glomeruli, leading to a range of symptoms and complications. There are many different types of glomerulonephritis, which can be classified based on their underlying cause. Some common causes include infections (such as strep throat or hepatitis B), autoimmune disorders (such as lupus or rheumatoid arthritis), and certain medications or toxins. Symptoms of glomerulonephritis can vary depending on the severity and underlying cause of the condition. Common symptoms may include blood in the urine, swelling in the legs or feet, high blood pressure, fatigue, and changes in urine output. Treatment for glomerulonephritis typically involves managing symptoms and addressing the underlying cause of the inflammation. This may include medications to reduce inflammation, control blood pressure, and prevent further damage to the kidneys. In some cases, more aggressive treatments such as dialysis or kidney transplantation may be necessary.

B-Cell Activation Factor Receptor (BAFF-R) is a protein receptor found on the surface of B cells, a type of white blood cell that plays a crucial role in the immune system. BAFF-R is activated by the binding of the protein BAFF (B-Cell Activating Factor of the TNF Family), which is produced by various cells in the body, including immune cells and epithelial cells. When BAFF binds to BAFF-R, it triggers a signaling cascade within the B cell that leads to the activation, proliferation, and differentiation of the B cell. This process is essential for the production of antibodies, which are proteins that help the immune system recognize and neutralize foreign substances such as viruses and bacteria. Disruptions in the regulation of BAFF-R signaling have been implicated in several autoimmune diseases, including lupus and rheumatoid arthritis, where the immune system mistakenly attacks healthy cells and tissues. Therefore, targeting BAFF-R signaling has become a promising therapeutic strategy for the treatment of these diseases.

CD4 antigens, also known as CD4 molecules, are a type of protein found on the surface of certain cells in the immune system. These cells, called T cells, play a crucial role in the body's defense against infection and disease. CD4 antigens are specifically associated with helper T cells, which are a type of T cell that works to coordinate the immune response by activating other immune cells. Helper T cells express high levels of CD4 antigens on their surface, which allows them to bind to and activate other immune cells, such as B cells and macrophages. In the context of the human immunodeficiency virus (HIV), the virus specifically targets and destroys CD4+ T cells, leading to a weakened immune system and an increased susceptibility to opportunistic infections and certain types of cancer. Therefore, CD4+ T cell count is often used as a key indicator of HIV infection and disease progression.

Alopecia areata is a type of hair loss that occurs when the immune system attacks the hair follicles, causing them to stop producing hair. It is a non-scarring form of hair loss, meaning that the hair follicles are not damaged and can eventually produce hair again. Alopecia areata can affect people of all ages and ethnicities, and it can affect any part of the body, although it most commonly affects the scalp. The severity of alopecia areata can vary widely, from small, round bald patches to complete hair loss on the scalp and body. There is no known cure for alopecia areata, but there are treatments available that can help to slow or stop hair loss and promote hair regrowth. These treatments may include corticosteroids, immunosuppressive drugs, and hair growth products. In some cases, hair loss may be permanent, but most people with alopecia areata are able to regrow their hair eventually.

CD95, also known as Fas or Apo-1, is a cell surface protein that plays a role in the regulation of immune responses and cell death. Antigens, CD95 refers to molecules that bind to the CD95 protein on the surface of immune cells, triggering a cascade of events that can lead to cell death. This process is known as apoptosis and is an important mechanism for eliminating damaged or infected cells from the body. CD95 antigens are also involved in the regulation of immune responses, including the activation and differentiation of T cells and B cells. In the medical field, CD95 antigens are often studied as potential targets for the treatment of various diseases, including cancer, autoimmune disorders, and viral infections.

CD80 is a protein that is expressed on the surface of certain cells in the immune system, including antigen-presenting cells (APCs) such as dendritic cells and macrophages. CD80 is also known as B7-1, and it plays a critical role in the activation of T cells, which are a type of immune cell that helps to fight off infections and diseases. When an APC encounters a pathogen, it engulfs the pathogen and processes its antigens, which are small pieces of the pathogen that can be recognized by the immune system. The APC then presents these antigens on its surface, along with the CD80 protein, to T cells. This interaction between the APC and the T cell is a key step in the activation of the T cell, which then becomes activated and begins to divide and differentiate into effector T cells that can directly attack the pathogen or into memory T cells that can provide long-term protection against future infections by the same pathogen. Antigens, CD80 are often used in medical research and as a tool for developing vaccines and other immune-based therapies. They can be used to stimulate the immune system to recognize and attack specific pathogens or cancer cells, or they can be used to suppress the immune system in cases where it is overactive or causing autoimmune diseases.

Pemphigus is a group of autoimmune diseases that cause blistering of the skin and mucous membranes. The word "pemphigus" comes from the Greek word "pemphix," which means blister. There are several types of pemphigus, including pemphigus vulgaris, pemphigus foliaceus, pemphigus barbae, and pemphigus vegetans. In pemphigus vulgaris, the immune system produces antibodies that attack the proteins that hold cells together in the skin and mucous membranes. This leads to the formation of blisters that can be painful and itchy. Pemphigus vulgaris can affect any part of the body, but it most commonly affects the skin on the face, scalp, and trunk. Pemphigus foliaceus is a milder form of pemphigus that primarily affects the skin. It is characterized by small, flat blisters that appear on the scalp, face, and trunk. Pemphigus barbae is a rare form of pemphigus that affects the beard area and is more common in men. Pemphigus vegetans is a rare form of pemphigus that causes large, raised blisters that can be painful and itchy. Treatment for pemphigus typically involves the use of medications to suppress the immune system and prevent further blistering. This may include corticosteroids, immunosuppressive drugs, and biologic therapies. In severe cases, hospitalization may be necessary.

Demyelinating autoimmune diseases of the central nervous system (CNS) are a group of disorders characterized by the loss of the protective myelin sheath that surrounds nerve fibers in the brain and spinal cord. This loss of myelin can lead to damage or dysfunction of the nerve fibers, resulting in a range of symptoms depending on the specific location and extent of the demyelination. The most well-known demyelinating autoimmune disease of the CNS is multiple sclerosis (MS), which is an inflammatory disorder that affects the myelin and the nerve fibers in the brain and spinal cord. Other demyelinating autoimmune diseases of the CNS include acute disseminated encephalomyelitis (ADEM), neuromyelitis optica (NMO), and optic neuritis. These diseases are considered autoimmune because they are caused by an abnormal immune response in which the body's immune system attacks its own tissues. In the case of demyelinating autoimmune diseases of the CNS, the immune system mistakenly attacks the myelin sheath, leading to inflammation and damage to the nerve fibers. Treatment for demyelinating autoimmune diseases of the CNS typically involves the use of immunosuppressive medications to reduce inflammation and slow the progression of the disease. In some cases, physical therapy and other supportive therapies may also be used to manage symptoms and improve quality of life.

In the medical field, a virus disease is a condition caused by a virus, which is a tiny infectious agent that can only replicate inside living cells. Viruses can infect a wide range of organisms, including humans, animals, plants, and even bacteria. When a virus enters the body, it attaches to and invades host cells, taking over the cell's machinery to produce more copies of itself. This can cause damage to the host cells and trigger an immune response, which can lead to symptoms such as fever, cough, sore throat, and fatigue. Some common examples of virus diseases in humans include the common cold, influenza, herpes simplex virus (HSV), human immunodeficiency virus (HIV), and hepatitis B and C. These diseases can range from mild to severe and can be treated with antiviral medications, vaccines, or supportive care.

Membrane glycoproteins are proteins that are attached to the cell membrane through a glycosyl group, which is a complex carbohydrate. These proteins play important roles in cell signaling, cell adhesion, and cell recognition. They are involved in a wide range of biological processes, including immune response, cell growth and differentiation, and nerve transmission. Membrane glycoproteins can be classified into two main types: transmembrane glycoproteins, which span the entire cell membrane, and peripheral glycoproteins, which are located on one side of the membrane.

Rheumatoid factor (RF) is an antibody that is produced by the immune system in response to certain types of infections or autoimmune diseases. In rheumatoid arthritis (RA), a chronic inflammatory disorder that affects the joints, RF is often present in the blood of affected individuals. RF is a type of immunoglobulin M (IgM) antibody that binds to the Fc portion of the immunoglobulin G (IgG) antibody. This binding can lead to the formation of immune complexes, which can deposit in the joints and other tissues, causing inflammation and damage. RF levels can be measured in the blood using a blood test. While the presence of RF is not diagnostic of RA, it is often used as a marker of disease activity and can be used to monitor the effectiveness of treatment. Additionally, some people with RA may have high levels of RF even after their symptoms have improved, indicating that the disease may not be in remission.

Systemic Scleroderma, also known as Scleroderma, is a chronic autoimmune disorder that affects the connective tissue in the body. It causes the skin and internal organs to become hard and inflexible, leading to a range of symptoms and complications. The exact cause of Systemic Scleroderma is not known, but it is believed to be triggered by an abnormal immune response that causes the body's own tissues to be attacked and damaged. The disease can affect people of all ages and ethnicities, but it is more common in women than in men. Symptoms of Systemic Scleroderma can vary widely depending on the severity and location of the disease. Common symptoms include skin thickening and hardening, Raynaud's phenomenon (a condition that causes the fingers and toes to turn white or blue when exposed to cold), joint pain and stiffness, digestive problems, and lung fibrosis (scarring of the lungs). Treatment for Systemic Scleroderma typically involves a combination of medications, physical therapy, and lifestyle changes. Medications may include immunosuppressants, corticosteroids, and disease-modifying antirheumatic drugs (DMARDs). Physical therapy can help to improve flexibility and reduce pain, while lifestyle changes such as quitting smoking and maintaining a healthy weight can help to slow the progression of the disease.

CD40 Ligand (CD40L) is a protein that is expressed on the surface of activated T cells, B cells, and dendritic cells. It plays a critical role in the immune response by binding to the CD40 receptor on the surface of antigen-presenting cells (APCs), such as dendritic cells and B cells. This interaction triggers a signaling cascade that leads to the activation and proliferation of APCs, as well as the differentiation of T cells into effector cells that can attack infected cells or cancer cells. CD40L is also involved in the regulation of inflammation and the development of autoimmunity. In the medical field, CD40L is being studied as a potential target for the treatment of various diseases, including cancer, autoimmune disorders, and infectious diseases.

Interleukin-4 (IL-4) is a type of cytokine, which is a signaling molecule that plays a crucial role in regulating the immune system. IL-4 is primarily produced by T-helper 2 (Th2) cells, which are a type of immune cell that helps to fight off parasitic infections and allergies. IL-4 has several important functions in the immune system. It promotes the differentiation of Th2 cells and stimulates the production of other Th2 cytokines, such as IL-5 and IL-13. IL-4 also promotes the activation and proliferation of B cells, which are responsible for producing antibodies. Additionally, IL-4 has anti-inflammatory effects and can help to suppress the activity of T-helper 1 (Th1) cells, which are involved in fighting off bacterial and viral infections. In the medical field, IL-4 is being studied for its potential therapeutic applications. For example, it is being investigated as a treatment for allergies, asthma, and certain autoimmune diseases. IL-4 is also being studied as a potential cancer immunotherapy, as it can help to activate immune cells that can recognize and attack cancer cells.

... "natural autoimmunity"). Autoimmunity should not be confused with alloimmunity. While a high level of autoimmunity is unhealthy ... a low level of autoimmunity may actually be beneficial. Taking the experience of a beneficial factor in autoimmunity further, ... Autoimmunity means presence of antibodies or T cells that react with self-protein and is present in all individuals, even in ... In immunology, autoimmunity is the system of immune responses of an organism against its own healthy cells, tissues and other ...
... is a bimonthly peer-reviewed medical journal publishing review articles pertaining to autoimmunity. It was ... "Autoimmunity Reviews". 2016 Journal Citation Reports. Web of Science (Science ed.). Clarivate Analytics. 2017. Official website ...
"About Autoimmunity". Retrieved 2010-01-20. "Paolo Casali Homepage". Retrieved 2010-01-20. v t e (Articles with short ... Autoimmunity is an international, peer-reviewed medical journal that covers the pathogenesis, immunology, genetics, and ... The editor in chief of Autoimmunity is Paolo Casali, the Donald L Bren Professor of Medicine, Molecular Biology & Biochemistry ...
Supplement on autoimmunity by Nature [1] Focus on autoimmunity by Nature Immunology [2] ISNI - International Society of ... Skepticism towards protective autoimmunity has been further fueled by the general concept of the CNS as being an immune ... Protective autoimmunity is a condition in which cells of the adaptive immune system contribute to maintenance of the functional ... The term 'protective autoimmunity' was coined by Prof. Michal Schwartz of the Weizmann Institute of Science (Israel), whose ...
The Journal of Autoimmunity is a peer-reviewed medical journal covering research on all aspects of autoimmunity. It was ... "Journal of Autoimmunity". 2021 Journal Citation Reports. Web of Science (Science ed.). Clarivate Analytics. 2022. Official ...
... (TAMA) is a severe often fatal disease that presents in some patients with thymoma. ... Wadhera A, Maverakis E, Mitsiades N, Lara PN, Fung MA, Lynch PJ (Oct 2007). "Thymoma-associated multiorgan autoimmunity: a ...
Bolz DD, Weis JJ (August 2004). "Molecular mimicry to Borrelia burgdorferi: pathway to autoimmunity?". Autoimmunity. 37 (5): ... One hypothesis is autoimmunity triggered by the infection, which may persist long-term after the triggering infection is ... Singh SK, Girschick HJ (July 2004). "Lyme borreliosis: from infection to autoimmunity". Clinical Microbiology and Infection. 10 ... Journal of Autoimmunity. 57: 82-115. doi:10.1016/j.jaut.2014.09.004. PMID 25451629. Weir W (19 September 2013). "Lyme Disease ...
Autoimmunity has been increasingly linked to targeted deregulation of epigenetic mechanisms, and therefore, use of epigenetic ... Research into the link between smell, depressive behavior, and autoimmunity has turned up interesting findings including the ... Sawalha A.H. (2008). "Epigenetics and T-cell immunity". Autoimmunity. 41 (4): 245-252. doi:10.1080/08916930802024145. PMID ... to autoimmunity and neurodegeneration. Other evidence has shown that development and deployment of the innate and acquired ...
Autoimmunity. 28 (1): 15-23. doi:10.3109/08916939808993841. PMID 9754810. van den Maagdenberg AM, Schepens JT, Schepens MT, et ...
Autoimmunity. 42 (3): 209-15. doi:10.1080/08916930802668610. PMID 19301202. S2CID 3135174. Liu C, Wei Y, Wang J, Pi L, Huang J ...
DQ mediates autoimmunity by skewing the T-cell receptor (TCR) repertoire during thymic selection. Carriers of risk serotypes ... form a regulatory T-cell population that protects self tissues from immune attack or autoimmunity. HLA-DQ (DQ) is encoded on ... Autoimmunity. 39 (4): 277-288. doi:10.1080/08916930600738581. PMID 16891216. S2CID 23462117. Fasano, Alessio (2011). "Dr". ... indicate that potentially a small change or increase in the presentation of a potential self-antigen can result in autoimmunity ...
Hyland KV, Engman DM (2006). "Further thoughts on where we stand on the autoimmunity hypothesis of Chagas disease". Trends in ... Franceschini F, Cavazzana I (February 2005). "Anti-Ro/SSA and La/SSB antibodies". Autoimmunity. 38 (1): 55-63. doi:10.1080/ ... Franceschini F, Cavazzana I (2005). "Anti-Ro/SSA and La/SSB antibodies". Autoimmunity. 38 (1): 55-63. doi:10.1080/ ... Strous RD, Shoenfeld Y (2006). "Schizophrenia, autoimmunity and immune system dysregulation: a comprehensive model updated and ...
Autoimmunity. 41 (7): 543-53. doi:10.1080/08916930802194195. PMID 18608174. S2CID 20611672. Maneglier B, Rogez-Kreuz C, ...
snRNP70 Migliorini P, Baldini C, Rocchi V, Bombardieri S (February 2005). "Anti-Sm and anti-RNP antibodies". Autoimmunity. 38 ( ...
Böhm I (May 2003). "Disruption of the cytoskeleton after apoptosis induction with autoantibodies". Autoimmunity. 36 (3): 183- ...
Autoimmunity. 67: 75-86. doi:10.1016/j.coi.2020.09.004. PMC 7744442. PMID 33176228. Welsh RM (August 2009). "Blimp hovers over ... BLIMP-1 is important in dampening autoimmunity, as well as antiviral and antitumor responses. BLIMP-1 regulates T cell ... cancer and autoimmunity". Nature Immunology. 22 (7): 809-819. doi:10.1038/s41590-021-00949-7. PMC 9197228. PMID 34140679. ...
Autoimmunity. 44 (3): 211-8. doi:10.3109/08916934.2010.530627. PMC 4465387. PMID 21231893. Kim JR, Horton NC, Mathew SO, Mathew ...
2002). "Smooth muscle antibodies and type 1 autoimmune hepatitis". Autoimmunity. 35 (8): 497-500. doi:10.1080/ ...
Autoimmunity. 29 (1): 33-42. doi:10.3109/08916939908995970. PMID 10052683. (Autoantibodies, PBC autoantibodies). ...
Niland B, Perl A (2004). "Evaluation of autoimmunity to transaldolase in multiple sclerosis". Autoimmunity. pp. 155-71. doi: ... Transaldolase is also a target of autoimmunity in patients with multiple sclerosis. Transaldolase is a single domain composed ...
"Autoimmunity". webMIC 419: Immunology. University of Arizona. Archived from the original on 2003-06-10. Green DR, Ware CF (June ... "Limited Peripheral T Cell Anergy Predisposes to Retinal Autoimmunity". The Journal of Immunology. 178 (7): 4276-4283. doi: ...
Autoimmunity. 40 (2): 148-160. doi:10.1080/08916930601183522. PMID 17453713. S2CID 20027248. Cristante E, McArthur S, Mauro C, ... or toxin-induced demyelination rather than autoimmunity." The four identified patterns are: Pattern I The scar presents T-cells ...
Autoimmunity. 49 (7): 496-502. doi:10.3109/08916934.2016.1167192. PMID 27050808. S2CID 23831262. v t e (Orphaned articles from ...
Autoimmunity. 22 (1): 33-42. doi:10.3109/08916939508995297. PMID 8882420. Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, Suyama A ...
Journal of Autoimmunity. 19 (4): 251-7. doi:10.1006/jaut.2002.0622. PMID 12473246. Park Y, Park H, Yoo E, Kim D (Nov 2003). " ... Autoimmunity. 33 (2): 95-101. doi:10.3109/08916930108995994. PMID 11264788. S2CID 43867785. Lampasona V, Scirpoli M, Bosi E, ...
Autoimmunity. 39 (1): 31-9. doi:10.1080/08916930500484674. PMID 16455580. S2CID 16987808. Kemeny, E; Grieve, T; Marcus, R; ... Autoimmunity Reviews. 21 (12): 103209. doi:10.1016/j.autrev.2022.103209. ISSN 1568-9972. PMID 36228998. S2CID 252865544. ... Autoimmunity. 39 (1): 31-39. doi:10.1080/08916930500484674. ISSN 0891-6934. PMID 16455580. S2CID 16987808. Guilherme, L; Kalil ...
Zieve, GW; Khusial, PR (September 2003). "The anti-Sm immune response in autoimmunity and cell biology". Autoimmunity Reviews. ... Mackay, IR; Whittingham, S; Fida, S; Myers, M; Ikuno, N; Gershwin, ME; Rowley, MJ (April 2000). "The peculiar autoimmunity of ... Damoiseaux, JG; Tervaert, JW (January 2006). "From ANA to ENA: how to proceed?". Autoimmunity Reviews. 5 (1): 10-7. doi:10.1016 ... Migliorini, P; Baldini, C; Rocchi, V; Bombardieri, S (February 2005). "Anti-Sm and anti-RNP antibodies". Autoimmunity. 38 (1): ...
Autoimmunity. 26 (2): 95-101. doi:10.3109/08916939709003852. PMID 9546818. Lara-Marquez M, Yunis J, Layrisse Z, Ortega F, ...
February 2014). "Coxsackievirus B1 is associated with induction of β-cell autoimmunity that portends type 1 diabetes". Diabetes ... Stratton, Richard; Slapak, Gabrielle; Mahungu, Tabitha; Loes, Sabine Kinloch-de (2009). "Autoimmunity and HIV". Current Opinion ... Shapira, Yinon; Agmon-Levin, Nancy; Shoenfeld, Yehuda (2009). "Mycobacterium Tuberculosis, Autoimmunity, and Vitamin D". ... 2001). "Echovirus 4 and type 1 diabetes mellitus". Autoimmunity. 34 (4): 275-81. doi:10.3109/08916930109014696. PMID 11905853. ...
Tian J, Lu Y, Zhang H, Chau CH, Dang HN, Kaufman DL (2004). "Gamma-aminobutyric acid inhibits T cell autoimmunity and the ... Autoimmunity. 44 (6): 465-70. doi:10.3109/08916934.2011.571223. PMC 5787624. PMID 21604972. Bhandage AK, Jin Z, Korol SV, Shen ...
Probiotics given to infants under 3 months of age appear to reduce the incidence of islet-cell autoimmunity by one-third, ... Islet-cell autoimmunity was found in 575 infants, 7.7% of the total. When stratified by country, 6.3% of subjects in the United ... "Our data show that the early introduction of probiotics may decrease the risk of islet autoimmunity. We found a one-third ... "We also know from previous studies that the incidence of islet autoimmunity is higher in Finland and Sweden compared with the ...
... a type of helper T cell involved in autoimmunity. The finding reveals potential new targets for treating autoimmune diseases. ... The Origins of Autoimmunity-Causing T Cells. Immune cells in the mouse spleen, a site of Th17 development. Helper T cells are ... Researchers discovered a new pathway for the development of Th17 cells, a type of helper T cell involved in autoimmunity. The ... that dampen the inflammatory response and help prevent autoimmunity. ...
Definition: Autoimmunity. Autoimmunity. The immune system defends the body against infections and certain other diseases. It is ... This is called autoimmunity. One example of an autoimmune disease is type 1 diabetes, in which the immune system destroys the ...
Single-cell immune repertoire sequencing of B and T cells in murine models of infection and autoimmunity. *Danielle Shlesinger1 ... Skin and gut imprinted helper T cell subsets exhibit distinct functional phenotypes in central nervous system autoimmunity. Nat ... Single-cell immune repertoire sequencing of B and T cells in murine models of infection and autoimmunity ... Myeloid-derived suppressor cells control B cell accumulation in the central nervous system during autoimmunity. Nat Immunol. ...
Autoimmunity and Inflammation in Myelodysplastic Syndromes. Autoimmunity and Inflammation in Myelodysplastic Syndromes. Journal ...
... infection and autoimmunity related to type 1 diabetes development in children and adolescents, according to a research letter ... Study suggests enterovirus infections linked with autoimmunity that leads to type 1 diabetes. Jan 9, 2017 ... Higher weight in first year may up risk of islet autoimmunity. Mar 30, 2016 ... "Long-term follow-up of persons with preexisting autoimmunity is necessary to determine whether SARS-CoV-2 accelerates ...
... Monday, 17 May 2021 ... Call for application for the seventh global crowdsourcing project with Merck, Regulatory T Cell Dysfunction in Autoimmunity ... Keywords: Autoimmunity; Inflammation; Aging; Biomedical Research; Drug Discovery; Academies and Institutes; Intersectoral ... and autoimmunity (intestinal epithelial barrier in autoimmune diseases). The next joint global crowdsourcing project will ...
We will focus on how dendritic cell subsets change the balance between major players in autoimmunity, namely Th1, Th17 and ... Autoimmunity results from the dysregulation of the immune system leading to tissue damage. Th1 and Th17 cells are known to be ... in the cytokine microenvironment and may be responsible for modulation of the inflammation and protection from autoimmunity. ... Autoimmunity results from the dysregulation of the immune system leading to tissue damage. Th1 and Th17 cells are known to be ...
"Autoimmunity" refers to a category of health conditions characterized by the immune system inappropriately attacking the ... "Clinical effect of IRT-⁠5 probiotics on immune modulation of autoimmunity or alloimmunity in the eye." Nutrients. Vol. 9, No. ... Supplementation with selected natural health products may have a role in the management of various conditions of autoimmunity. ... Several natural health products have been shown to modulate immune function and reduce inflammation in autoimmunity: probiotics ...
If confirmed, these results could lead to the development of a therapy whereby T-Cells that suppress autoimmunity can be ... Studies On Regen BioPharma, Inc.s DURACAR Indicate Potential Suppression Of Autoimmunity, Company Retains Contract Research ... www.prnewswire.com/news-releases/studies-on-regen-biopharma-incs-duracar-indicate-potential-suppression-of-autoimmunity-company ...
When this happens, your body develops a reaction that can lead to autoimmunity. ... Autoimmunity: Why the Body Attacks Itself. Posted on November 15, 2016 by Frontiers Communications in Young Minds // 0 Comments ... When this happens, your body develops an allergic reaction or inflammation that can lead to something called autoimmunity. ... When this happens, your body develops a reaction that can lead to autoimmunity. ...
Autoimmunity. Much evidence supports the hypothesis that alopecia areata is an autoimmune condition. The process appears to be ... Clinical evidence favoring autoimmunity suggests that alopecia areata is associated with other autoimmune conditions, the most ... Studies in humans also reinforce the hypothesis of autoimmunity. Studies have shown that hair regrows when affected scalp is ...
The technical storage or access that is used exclusively for statistical purposes. The technical storage or access that is used exclusively for anonymous statistical purposes. Without a subpoena, voluntary compliance on the part of your Internet Service Provider, or additional records from a third party, information stored or retrieved for this purpose alone cannot usually be used to identify you. ...
Autoantibodies Autoimmunity Child Child, Preschool Diabetes Mellitus, Type 1 Dietary Supplements Fatty Acids, Omega-3 Female ... "Maternal Dietary Supplement Use and Development of Islet Autoimmunity in the offspring: the TEDDY Study" vol. 20, no. 1, 2018. ... 2018). Maternal Dietary Supplement Use and Development of Islet Autoimmunity in the offspring: the TEDDY Study. 20(1). Silvis, ... "Maternal Dietary Supplement Use and Development of Islet Autoimmunity in the offspring: the TEDDY Study" 20, no. 1 (2018). ...
WD 305 2006PR Principles and methods for assessing autoimmunity associated with exposure to chemicals. WD 305 94AU Autoimmunity ... TextPublication details: New York : Wiley-Liss, 1994. Description: 459 pISBN: 0471592277Subject(s): Autoimmunity -- physiology ... Autoimmunity : physiology and disease / editors, Antonio Coutinho, Michel D. Kazatchkine. Contributor(s): Coutinho, Antonio , ...
Cite this: The HPV Vaccine and Autoimmunity: Reviewing the Research - Medscape - Sep 15, 2016. ... not found evidence that meets any of the four operational criteria necessary to prove that HPV vaccines induce autoimmunity. ... not found evidence that meets any of the four operational criteria necessary to prove that HPV vaccines induce autoimmunity. ...
... submitted by: admin on 02/20/2015. Autoimmunity is preventable and treatable, usually without drugs. Modern ...
... Autoimmune diseases affect over 1 million Australians and are a leading cause of death in women under the age of ...
... may be seeing a rise in autoimmunity, especially among adolescents. ... Autoimmunity in adolescents tripled in recent decades. Protein increase in blood could predict future autoimmune diseases. In ... The rise in autoimmunity is linked to a certain type of antibody in the blood. Antibodies are proteins that the immune system ... Autoimmunity, which is when the immune system attacks the body instead of protecting it against disease, appears to be rising ...
Drug-Induced Autoimmunity - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD Manuals - Medical ...
Autoimmunity What Causes Autoimmunity and How to Treat It What is an autoimmune disease? An autoimmune disease is a condition ...
I feel very passionately about autoimmunity as there is so much can be done to take back control of your health once you have ... In autoimmunity, we are led to believe the immune system gradually mistakenly attacks the bodys own tissue, creating ... It wasnt my intention to specialize in gut health and autoimmunity. It has happened this way partly because of my own ... Addressing the underlying immune system disturbance in autoimmunity is rarely as simple as identifying a single magic bullet ...
Autoimmunity [see WARNINGS AND PRECAUTIONS]. Clinical Trials Experience. Because clinical trials are conducted under widely ... Autoimmunity. Treatment with adalimumab products may result in the formation of autoantibodies and, rarely, in the development ... No patient developed clinical signs of autoimmunity during the clinical trial.. Approximately 15% of patients treated with ...
All is One autoimmunity Being Still changing your thinking gratitude Judging mind body connection Self-rejecting Read more ... Besting Autoimmunity Its too easy to get stuck in a loop of anger, resentment, fear and defeat by an autoimmune condition. ...
published correction appears in Autoimmunity. 2006 Jun;39(4):349. Swindt, Christina [corrected to Schwindt, Christina]]. ... Autoimmunity. 2006;39(2):137-141. Accessed May 13, 2021.. 13Zee PC, Turek FW. Sleep and health: Everywhere and in both ...
These cells dampen immune responses and curb autoimmunity - by, for example, ramping up the production of regulatory molecules ... Regulation of allergy and autoimmunity in helminth infection. Clin Rev Allergy Immunol. 2004 Feb;26(1):35-50. Review View ...
To best support you on your journey to overcoming your personal challenges with autoimmunity, I am here to walk with you step ... If you are living with daily challenges of autoimmunity like fatigue, brain fog, digestion issues or unhealthy weight changes, ... To help you overcome your personal challenges with autoimmunity, and finally achieve the goals you have for your health, I ... and I have helped them successfully overcome daily challenges of autoimmunity by implementing personalized nutrition and ...
If youre reading this article, chances are you have an autoimmune disease or know someone who does. These chronic conditions, once considered rare, have exploded in the last 30 years. Part of this is due to a better understanding of the over 80 autoimmune diseases in general and their symptoms. Which, up until recently, were …. The Functional Medicine Solution for Autoimmune Disease Read More ». ...
Save my name, email, and website in this browser for the next time I comment ...
  • As the editors imply in their introduction, the relationship of infection and autoimmunity is complex, compelling, and best viewed as a physiologic process and potential consequence of normal immune recognition and immunoregulation. (cdc.gov)
  • There appears to be no association between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and autoimmunity related to type 1 diabetes development in children and adolescents, according to a research letter published online Aug. 5 in the Journal of the American Medical Association . (medicalxpress.com)
  • In the investigation led by Dr. Uusitalo, the researchers wanted to test the hypothesis that early probiotic exposure might be associated with reduced risk for islet-cell autoimmunity. (medscape.com)
  • Islet-cell autoimmunity was found in 575 infants, 7.7% of the total. (medscape.com)
  • Evidence of islet cell autoimmunity in elderly patients with type 2 diabetes. (cdc.gov)
  • Islet cell autoimmunity in triethnic adult population of the third National Health and Nutrition Examination Survey. (cdc.gov)
  • Therapeutic Benefits of Regulating Inflammation in Autoimmunity" by Enayat Nikoopour, Jordan Ari Schwartz et al. (uwo.ca)
  • Several natural health products have been shown to modulate immune function and reduce inflammation in autoimmunity: probiotics, vitamin D, and eicosapentaenoic acid (EPA) from fish oil. (newrootsherbal.com)
  • While the pathogenesis of AICs is incompletely understood, growing appreciation of cellular immune deregulation, cytokine hypersecretion, and the genetic heterogeneity underlying MDS may improve our understanding of common pathways linking MDS, inflammation, and autoimmunity. (aamds.org)
  • Previously it was known that microRNAs were important for the development of a subset of helper T cells called regulatory T cells, which are required to regulate the immune response and prevent attacks against host tissue that lead to autoimmunity. (rvc.ac.uk)
  • The next joint global crowdsourcing project will explore mechanisms of immune senescence and mitochondrial dysfunction in regulatory T cells and other T cell subsets that are shared in human autoimmunity and aging. (b3cnewswire.com)
  • Autoimmunity results from the dysregulation of the immune system leading to tissue damage. (uwo.ca)
  • Autoimmunity" refers to a category of health conditions characterized by the immune system inappropriately attacking the person's own body. (newrootsherbal.com)
  • Autoimmunity occurs when your immune system gets confused and your own tissue gets caught in friendly crossfire. (jennythehealthcoach.com)
  • Autoimmunity, which is when the immune system attacks the body instead of protecting it against disease, appears to be rising in the U.S. (medlineplus.gov)
  • As of 2022, 485 different types of PI had been described, affecting different components of the immune system and resulting in a variety of disorders, including increased susceptibility to severe infections and autoimmunity. (cdc.gov)
  • Under the new agreement, Merck will start up to six additional research projects at the BioMed X Institute, building on ongoing research projects in the fields of oncology (DNA damage response and RNA splicing) and autoimmunity (intestinal epithelial barrier in autoimmune diseases). (b3cnewswire.com)
  • Patients with LAD-1 are prone to develop autoimmune diseases, but the molecular and cellular mechanisms that result in coexisting immunodeficiency and autoimmunity are still unresolved. (jci.org)
  • The concept that islet autoimmunity results from genetic susceptibility combined with an environmental trigger, first theorised by Eisenbarth [ 10 ], is now generally accepted [ 11 ]. (springer.com)
  • Purkinje cytoplasmic autoantibody type 1 ( PCA -1)/anti-Yo autoimmunity is a common high- risk paraneoplastic neurological disorder , traditionally attributed antigenically to cerebellar degeneration-related protein 2 (CDR2), predominantly affecting women with gynecologic or breast adenocarcinoma . (bvsalud.org)
  • Cite this: The HPV Vaccine and Autoimmunity: Reviewing the Research - Medscape - Sep 15, 2016. (medscape.com)
  • We will focus on how dendritic cell subsets change the balance between major players in autoimmunity, namely Th1, Th17 and regulatory T cells. (uwo.ca)
  • Researchers discovered a new pathway for the development of Th17 cells, a type of helper T cell involved in autoimmunity. (nih.gov)
  • The discovery of IL-23 as a driving force in Th17 development points to potential new targets for therapies against autoimmunity. (nih.gov)
  • Our findings suggest that the small molecule FGIN-1-27 can be re-purposed to relieve autoimmunity by metabolic reprogramming of pathogenic Th17 cells. (listlabs.com)
  • Infants who are at genetic risk of developing type 1 diabetes and who were given probiotics before 3 months of age had a 33% reduction in the risk of pancreatic beta-cell islet autoimmunity, according to new results from an ongoing international study in over 7000 children. (medscape.com)
  • Type 1 diabetes results from the poorly understood process of islet autoimmunity, which ultimately leads to the loss of functional pancreatic beta cells. (springer.com)
  • Type 1 diabetes results from organ-specific autoimmunity, which eliminates most of the insulin-producing pancreatic beta cells. (springer.com)
  • However, at what stage in the progression toward clinical T2D does islet autoimmunity emerge as an important component influencing β-cell dysfunction? (frontiersin.org)
  • Call for application for the seventh global crowdsourcing project with Merck, 'Regulatory T Cell Dysfunction in Autoimmunity and Inflammaging' to open now. (b3cnewswire.com)
  • Here, we draw upon studies that have shed light on the initiation and progression of islet autoimmunity from the point of view of the beta cell. (springer.com)
  • Long-term follow-up of persons with preexisting autoimmunity is necessary to determine whether SARS-CoV-2 accelerates progression to clinical diabetes," the authors write. (medicalxpress.com)
  • We undertook this study to investigate the occurrence of and risk factors for severe infections in off-trial patients using data from the AutoImmunity and Rituximab (AIR) registry. (nih.gov)
  • Researchers speculate that the dysfunctional complement system is unable to distinguish what it should attack, and it sometimes attacks normal tissues, leading to autoimmunity. (medlineplus.gov)
  • Our data show that the early introduction of probiotics may decrease the risk of islet autoimmunity. (medscape.com)
  • Asked to comment on the data, Outi Vaarala, MD, research director at the Institute of Clinical Medicine, University of Helsinki, Finland, said: "The results of the study by Dr. Uusitalo, if reproduced in another observational study, suggest that an intervention with probiotics could be reasonable for the prevention of beta-cell autoimmunity. (medscape.com)
  • A pilot study we conducted in 2003 in Linköping, Sweden, tested the feasibility of probiotics in the prevention of beta-cell autoimmunity, and the results showed that there were no adverse effects and it was a safe intervention," she told Medscape Medical News . (medscape.com)
  • Undoubtedly, sustained efforts by the global type 1 diabetes research community to understand the basis of T cell-driven autoimmunity in type 1 diabetes have paid dividends. (springer.com)
  • Notwithstanding this achievement, we are still far from a nuanced understanding of how islet autoimmunity originates and propagates during the development of type 1 diabetes and why it is so heterogeneous among individuals. (springer.com)
  • We advance the hypothesis that antigen presentation by beta cells, their stress responses and functional heterogeneity are critical factors that will provide clues towards solving the enigma posed by islet autoimmunity in type 1 diabetes. (springer.com)
  • Central to solving the puzzle as to how type 1 diabetes occurs will be to identify the elusive cause(s) of initial islet autoimmunity. (springer.com)
  • The rise in autoimmunity is linked to a certain type of antibody in the blood. (medlineplus.gov)
  • However, this section lacks a review or balanced discussion of the various mechanisms of autoimmunity and proof of causation. (cdc.gov)
  • However, TGF-beta also drives the development of other T cells (regulatory T cells) that dampen the inflammatory response and help prevent autoimmunity. (nih.gov)
  • To understand the role of Treg in LAD-1 development and manifestation of autoimmunity, we generated mice specifically lacking CD18 on Treg (CD18Foxp3), resulting in defective LFA-1 expression. (jci.org)
  • Marian Rewers, M.D., Ph.D., from the Barbara Davis Center for Diabetes at the University of Colorado in Aurora, and colleagues offered a cross-sectional screening for islet autoantibodies and SARS-CoV-2 antibodies to children and adolescents aged 1 to 18 years participating in the Autoimmunity Screening for Kids study in Colorado and to children aged 1 to 10.9 years from the Frida study in Bavaria, Germany. (medicalxpress.com)
  • New research funded by the National Institutes of Health (NIH) found that autoimmunity is increasing faster in males, non-Hispanic whites, adults 50 years and older, and adolescents. (medlineplus.gov)
  • Mounting evidence supports the notion that the activation and evolution of islet autoimmunity in genetically susceptible people is contingent upon early life exposures affecting the islets, especially beta cells. (springer.com)
  • We found a one-third reduction in the incidence of islet autoimmunity, and this is high," she said. (medscape.com)
  • To date, researchers have not found evidence that meets any of the four operational criteria necessary to prove that HPV vaccines induce autoimmunity. (medscape.com)
  • When this happens, your body develops a reaction that can lead to autoimmunity. (frontiersin.org)
  • When this happens, your body develops an allergic reaction or inflammation that can lead to something called autoimmunity. (frontiersin.org)
  • We also know from previous studies that the incidence of islet autoimmunity is higher in Finland and Sweden compared with the US. (medscape.com)
  • While the role of islet autoimmunity remains unquestioned, the role of the islets as active participants has only recently become accepted [ 1 ]. (springer.com)
  • CD4+FOXP3+ Treg are known for their essential role in preventing autoimmunity. (jci.org)
  • The researchers want to know what is causing these changes in autoimmunity in each of the groups, especially teenagers. (medlineplus.gov)